Fossil Hominids: mitochondrial DNA
In July 1997, the first successful extraction of Neandertal DNA was announced. In an article in the journal Cell, a team of German and American researchers led by Svante Pääbo (Krings et al. 1997) claimed to have extracted mitochondrial DNA (mtDNA) from a piece of bone cut from the upper arm of the first recognised Neandertal fossil, the individual found at the Feldhofer grotto in the Neander Valley in Germany in 1856 (Kahn and Gibbons 1997, Ward and Stringer 1997). What is the significance of this study?
What is mitochondrial DNA?
DNA (deoxyribonucleic acid) is the gigantic molecule which is used to encode genetic information for all life on Earth. DNA molecules consists of a long strand of base molecules arranged in the form of a double helix. The bases are adenine, guanine, cytosine, and thymine, often abbreviated as A, G, C, and T. What we ordinarily think of as "our" DNA, because it controls most aspects of our physical appearance, is also known as "nuclear DNA", because every cell in our bodies contains two copies of it in the cell nucleus.
Mitochondria (singular: mitochondrion) are small energy-producing organelles found in cells. Surprisingly, mitochondria have their own DNA molecules, entirely separate from our nuclear DNA. Most cells contain between 500 and 1000 copies of the mtDNA molecule, which makes it a lot easier to find and extract than nuclear DNA. In humans the mtDNA genome consists of about 16,000 base pairs (far shorter than our nuclear DNA), and has been completely sequenced (for one individual, at least; Anderson et al. 1981). What makes mtDNA particularly interesting is that, unlike nuclear DNA which is equally inherited from both father and mother, mtDNA is inherited only from the mother, because all our mitochondria are descended from those in our mother's egg cell (there may be exceptions to this rule, however; see below).
Mitochondrial Eve
The concept of "mitochondrial Eve" is widely misunderstood. It does not mean that she was the only woman of her time who was ancestral to modern humans. In other words, mitochondrial Eve was not a Biblical Eve. However the Biblical Eve, if she had existed, might well be mitochondrial Eve (though not necessarily: it could be one of her female descendants). Read What is a mitochondrial Eve? for an exact definition and a good explanation of the concept.
Consider the set of all women living today, then the set of all their mothers, and so on. Obviously, each set will be as small as or smaller than the previous set. Eventually the set will contain only one woman, who is known as "mitochondrial Eve". The mtDNA of all living humans is inherited from mitochondrial Eve.
Normally our mtDNA is identical to that of our mother. But, like all DNA, mtDNA mutates occasionally so that one of the bases (A, C, G, or T) changes to a different base. Because of these mutations, human mtDNA has been slowly diverging from the mtDNA of mitochondrial Eve, and the amount of mutation is roughly proportional to the amount of time that has passed. This means that similarity of mtDNA for any two humans provides a rough estimate of how closely they are related through their maternal ancestors. If they have identical mtDNA, they are fairly closely related, maybe even siblings. If they have very different mtDNA, it means their last common maternal ancestor lived long ago.
However, using the genetic difference to estimate the time of the last common ancestor is difficult, for a couple of reasons. One is that the rate at which mtDNA mutates is poorly measured. The other is that even if the average mutation rate is accurately known, some lineages will as a matter of chance accumulate fewer or more mutations than average.
Extraction of the mitochondrial DNA
After death, DNA starts degrading immediately. It is thought that under the most favorable conditions, some DNA fragments can survive for as long as 50,000 to 100,000 years. The Feldhofer Neandertal fossil, thought to be between 30,000 and 100,000 years old, was therefore pushing the limits for this kind of work. However initial testing of the fossil showed good preservation of amino acids, indicating that it might contain recoverable mtDNA.
Polymerase Chain Reaction (PCR) is a technique which can be used to create many copies of an initially small number of molecules. The researchers used PCR to amplify and extract many short strands of mtDNA from the Neandertal sample. By overlapping these, they were able to generate a sequence of 379 bases apparently from the Neandertal individual. To protect against errors and contamination, each base was extracted in at least two separate amplifications.
Krings et al. then compared this sequence against a database of 994 different mtDNA sequences from modern humans. For the sequence of mtDNA in question, humans on average differ from each other in 8 +/- 3.1 positions (the '3.1' represents one standard deviation). The greatest difference between any two modern humans was 24, and the smallest difference was 1 (because duplicates were removed from the database).
Distributions of Pairwise Sequence Differences among Humans, the Neandertal, and Chimpanzees.
X axis, the number of sequence differences; Y axis, the percent of pairwise comparisons. (Krings et al, 1997)
By contrast, the Neandertal genome had an average of 27 +/- 2.2 differences from modern humans (3.375 times the average difference between modern humans). The smallest difference between any human and the Neandertal was 22, and the largest difference between any human and the Neandertal was 36. These differences put the Neandertal genome well outside the limits of modern humans. Another interesting result is that the mtDNA sequence seemed equally distant from all modern groups of humans. In particular, it did not seem to be more closely related to Europeans, something that might have been expected if, as some scientists think, Neandertals were at least partly ancestral to them.
In 1999, the same workers successfully extracted a second sequence of 340 base pairs of mtDNA from the same Neandertal fossil (Krings et al. 1999). This study confirmed the results of the first. When differences were calculated between the 600 comparable base pairs of 663 modern humans, the Neandertal, and 9 chimpanzees, modern humans differed from each other by 10.9 +/- 5.1 (range 1-35), the Neandertal differed from humans by 35.3 +/- 2.3 (range 29-43), and humans and the two Neandertals both differed from chimps by about 94.
mtDNA from a second Neandertal
In 1999, scientists successfully extracted a 345 base pair sequence of mtDNA from a second Neandertal, a 29,000 year-old fossil of a baby recently discovered in Mesmaiskaya cave in south-western Russia. (Ovchinnikov et al. 2000, Höss 2000) The results of this study were similar to the previous ones, putting the Mezmaiskaya specimen outside the range of modern human mtDNA.
In addition, the two Neandertals are fairly similar, differing from each other in 12 base pairs. The difference is greater than that usually found between pairs of modern Europeans or Asians (only 1% of whom differ in 12 or more places), but comparable to the differences between modern Africans (37% of whom differ by 12 or more).
The distance between Mezmaiskaya and a particular modern human sequence known as the reference sequence (Anderson et al. 1981) was 22, compared to 27 for the first Neandertal. (However, no figures are given for the minimum, average and maximum distances between Mezmaiskaya and modern humans; it is unclear whether Mezmaiskaya is in general closer to modern humans than Feldhofer is.)
The phylogenetic analyses of Ovchinnikov et al. show the two Neandertals grouped together, and separated from all modern humans. As with the first specimen, Mezmaiskaya also appears to be equidistant from all groups of modern humans, strengthening the conclusion that Neandertals are not closely related to modern Europeans.
Because this second individual was discovered about 2,500 km (1,500 miles) from the first, it provides very strong confirmation of the previous results.
The fact that its mtDNA was also fairly close to that of the first Neandertal makes it much less likely that Neandertals and the ancestors of modern humans were both part of an interbreeding population with a large amount of mtDNA genetic variation that has been mostly lost:
"In particular, these data reduce the likelihood that Neanderthals contained enough mtDNA sequence diversity to encompass modern human diversity" (Ovchinnikov et al. 2000)
Interestingly, the preservation of the Mezmaiskaya specimen appears to be much better than that of the Feldhofer specimen. It is so good, in fact, that there is a possibility that its entire mtDNA genome may be able to be sequenced, and there is even a possibility that some of its nuclear DNA may be retrievable.
mtDNA from a third Neandertal
In 2000, scientists announced the sequencing of a third Neandertal mtDNA specimen from a cave at Vindija, Croatia (Krings et al. 2000). When the three Neandertals are compared with modern humans, all three of them cluster together, and apart from all modern humans. This conclusion is reinforced by a study by Knight (2003). Knight excluded from the comparison sites in the mtDNA genome which are known to have mutated more than once, and which are therefore poor indicators of phylogenetic relationships. His study strongly confirmed earlier ones showing deeply divergent histories for modern human mtDNA lineages and the known Neandertal ones.
Like modern humans, Neandertals had low genetic diversity compared to apes. The diversity of the three Neandertal mtDNA sequences (3.73%) is lower than that of chimpanzees (14.82+/-5.7%) and gorillas (18.57+/-5.26%), and similar to that of modern humans worldwide (3.43+/-1.22%). If modern humans are sorted into continental groups, the diversity of the three Neandertals is similar to (within one standard deviation of) that for Africans, Asians, native Americans and Australian aboriginals, and Oceanians. Modern Europeans, who live in approximately the same region as the Neandertals, have less diversity than the Neandertals.
Still more Neandertal mtDNA
Schmitz et al. (2002) reported on a fourth Neandertal mtDNA sequence from the second Neandertal fossil found at Feldhofer, the site in Germany at which the first Neandertal fossil was found. It was closely related to the previous Neandertal mtDNA sequences.
Serre et al. (2004) were able to sequence mtDNA from four other Neandertal fossils, along with mtDNA from five early modern humans. The four Neandertals all had mtDNA similar to those found in the previous Neandertals. Serre and his colleagues found no evidence of mtDNA gene flow between modern humans and Neandertals in either direction, but could not rule out the possibility of limited gene flow. Interestingly, the mtDNA sequences from the Vindija Neandertals, which have a less extreme Neandertal anatomy than the classic Neandertals, and are considered transitional between modern humans and classic Neandertals by some scientists, were no closer to modern humans than the rest of the Neandertal fossils.
Is the Neandertal outside the human range?
Yes.
Note that because two modern human sequences are 24 bases apart, while the smallest Neandertal/human difference is only 22, does not mean the Neandertal sequence is within the range of modern humans. To use an analogy, suppose we measured the height of 994 adult humans, and they varied from 4'8" to 6'8" (a difference of 24 inches). Suppose we then found a skeleton which was 8'6" in height. No one would claim that it fell within the modern human range because it was closer to the nearest human (22 inches) than the tallest human was from the shortest human (24 inches).
Note also that the two figures (22 and 24) are measuring very different things, making it invalid to compare the two figures. Just as the Neandertal was compared against 994 modern humans, any of those humans could be similarly compared against the other 993 humans. We could compute the minimum, average, and maximum distance from that human to the other humans, just as was done for the Neandertal. If we calculated those values for all the humans, we could then calculate minimum, average and maximum values of all the individual minima, averages and maxima, and compare those values against the equivalent values for the Neandertal.
We do not know from the Krings et al. 1997 paper the distribution of minimum distances of humans from other humans. The smallest such value is 1. The largest such value might, I suspect, be as much as 5. The same value for the Neandertal is 22, well outside the human range.
For average distances of humans to other humans, we know the average value is 8.0. The minimum average distance will be a little less; the maximum average value must be at least 12 (this can be deduced from the fact that there are two humans 24 apart) and less than 24; I would guess it might be about 16 for a highly atypical human. For the Neandertal, the value is 27, again well outside the human range.
For maximum distances, the maximum such value is 24, but for most humans, the maximum distance to any other human will be less than that. The value of 24 is highly atypical, because it is taken between the two individuals who have indepently diverged farthest from mitochondrial Eve, and is the maximum of nearly half a million (994 * 993 / 2) comparisons among modern humans. For the Neandertal, the value is 36, again well outside the human range.
In other words, for all three measurements (minimum, average and maximum distances to other humans), the Neandertal measurement is much larger than the maximum value of the same measurement from a sample of 994 modern humans, and even further from the average value. The Neandertal is not merely outside the human range, but well outside it.
Possible problems
The use of mitochondrial mtDNA to investigate human history is not without drawbacks.
The rate of mtDNA mutation is not well known. A study by Parsons et al. (1997) found a rate 20 times higher than that calculated from other sources. In an article reviewing mtDNA research, Strauss (1999a) reports that mtDNA mutation rates differ in some groups of animals, and can even vary dramatically in single lineages. Although there are many agreements, some divergence dates for modern animals calculated from mtDNA do not match with what is known from the fossil record. There are suggestions from a few sources that paternal mtDNA can sometimes be inherited, which could affect analyses based on mtDNA.
In 1999 Awadalla et al. published a study suggesting that mtDNA could sometimes be inherited from fathers. If mtDNA is inherited only from mothers, the correlation between different mutations should not depend on how far apart on the genome they were. Instead, their measurements showed that mutations at distant sites on the mtDNA genome were less likely to be correlated than nearby mutations, suggesting that mtDNA from mothers and fathers could sometimes get mixed. However, there is no explanation so far as to how this recombination could be occurring, and the possibility that other phenomena could be causing this effect has not yet been disproved. If it occurs, mixing would mean that the dates from current mtDNA studies would be too old. If mixing is common enough, it could even mean that there was no mitochondrial Eve, because different parts of the mtDNA molecule would have different histories. (Awadalla et al. 1999, Strauss 1999b) Other studies, however, have contradicted these results and argued for strictly maternal mtDNA inheritance (Elson et al. 2001), and, according to Sykes (2001), the Awadalla paper and another paper which also suggested that mtDNA could be inherited paternally were based on incorrect data and were later retracted.
Conclusions
The studies of Neandertal mtDNA do not show that Neandertals did not or could not interbreed with modern humans. However, the lack of diversity in Neandertal mtDNA sequences, combined with the large differences between Neandertal and modern human mtDNA, strongly suggest that Neandertals and modern humans developed separately, and did not form part of a single large interbreeding population. The Neandertal mtDNA studies will strengthen the arguments of those scientists who claim that Neandertals should be considered a separate species which did not significantly contribute to the modern gene pool.
References
Anderson S., Bankier A.T., Barrel B.G., de Bruijn M.H.L., Coulson A.R., Drouin J. et al. (1981): Sequence and organization of the human mitochondrial genome. Nature, 290:457-74.
Awadalla P., Eyre-Walker A., and Smith J.M. (1999): Linkage disequilibrium and recombination in hominid mitochondrial DNA. Science, 286:2524-5.
Elson J.L., Andrews R.M., Chinnery P.F., Lightowlers R.N., Turnbull D.M., and Howell N. (2001): Analysis of European mtDNAs for recombination. American Journal of Human Genetics, 68:145-53.
Höss M. (2000): Neanderthal population genetics. Nature, 404:453-4.
Kahn P. and Gibbons A. (1997): DNA from an extinct human. Science, 277:176-8.
Knight A. (2003): The phylogenetic relationship of Neandertal and modern human mitochondrial DNAs based on informative nucleotide sites. Journal of Human Evolution, 44:627-32.
Krings M., Capelli C., Tschentscher F., Geisert H., Meyer S., von Haeseler A. et al. (2000): A view of Neandertal genetic diversity. Nature Genetics, 26:144-6.
Krings M., Geisert H., Schmitz R.W., Krainitzki H., and Pääbo S. (1999): DNA sequence of the mitochondrial hypervariable region II from the Neandertal type specimen. Proceedings of the National Academy of Sciences, USA, 96:5581-5.
Krings M., Stone A., Schmitz R.W., Krainitzki H., Stoneking M., and Pääbo S. (1997): Neandertal DNA sequences and the origin of modern humans. Cell, 90:19-30.
Ovchinnikov I.V., Götherström A., Romanova G.P., Kharitonov V.M., Lidén K., and Goodwin W. (2000): Molecular analysis of Neanderthal DNA from the northern Caucasus. Nature, 404:490-3.
Parsons T.J., Muniec D.S., Sullivan K., Woodyatt N., Alliston-Greiner R., Wilson M.R. et al. (1997): A high observed substitution rate in the human mitochondrial DNA control region. Nature Genetics, 15:363-8.
Schmitz R.W., Serre D., Bonani G., Feine S., Hillgruber F., Krainitzki H. et al. (2002): The Neandertal type site revisited: Interdisciplinary investigations of skeletal remains from the Neander Valley, Germany. Proceedings of the National Academy of Sciences, USA, 99:13342-7.
Serre D., Langaney A., Chech M., Teschler-Nicola M., Paunovic M., Mennecier P. et al. (2004): No evidence of Neandertal mtDNA contribution to early modern humans. PLoS Biology, 2:313-7.
Strauss E. (1999a): Can mitochondrial clocks keep time? Science, 283:1435
Strauss E. (1999b): mtDNA shows signs of paternal influence. Science, 286:2436
Sykes B. (2001): The seven daughters of Eve. London: Bantam Press. (a good popular book about mitochondrial DNA)
Ward R. and Stringer C.B. (1997): A molecular handle on the Neanderthals. Nature, 388:225-6.
Commentaries
Nature, feature of the week, March 30, 2000: Neanderthal DNA
Neandertal mitochrondrial sequence stored at GenBank (accession number AF011222)
DNA Shows Neandertals Were Not Our Ancestors (Pennsylvania State University)
DNA clues to Neanderthals: mtDNA from a third Neandertal
Neandertal DNA, by Mark Rose (Archaeological Institute of America)
Other references about mitochondrial DNA
Wednesday, December 3, 2008
Sunday, October 26, 2008
function of various brain waves
What is the function of the various brainwaves?It is well known that the brain is an electrochemical organ; researchers have speculated that a fully functioning brain can generate as much as 10 watts of electrical power. Other more conservative investigators calculate that if all 10 billion interconnected nerve cells discharged at one time that a single electrode placed on the human scalp would record something like five millionths to 50 millionths of a volt. If you had enough scalps hooked up you might be able to light a flashlight bulb.
Even though this electrical power is very limited, it does occur in very specific ways that are characteristic of the human brain. Electrical activity emanating from the brain is displayed in the form of brainwaves. There are four categories of these brainwaves, ranging from the most activity to the least activity. When the brain is aroused and actively engaged in mental activities, it generates beta waves. These beta waves are of relatively low amplitude, and are the fastest of the four different brainwaves. The frequency of beta waves ranges from 15 to 40 cycles a second. Beta waves are characteristics of a strongly engaged mind. A person in active conversation would be in beta. A debater would be in high beta. A person making a speech, or a teacher, or a talk show host would all be in beta when they are engaged in their work.
The Brainwaves
The next brainwave category in order of frequency is alpha. Where beta represented arousal, alpha represents non-arousal. Alpha brainwaves are slower, and higher in amplitude. Their frequency ranges from 9 to 14 cycles per second. A person who has completed a task and sits down to rest is often in an alpha state. A person who takes time out to reflect or meditate is usually in an alpha state. A person who takes a break from a conference and walks in the garden is often in an alpha state.
The next state, theta brainwaves, are typically of even greater amplitude and slower frequency. This frequency range is normally between 5 and 8 cycles a second. A person who has taken time off from a task and begins to daydream is often in a theta brainwave state. A person who is driving on a freeway, and discovers that they can't recall the last five miles, is often in a theta state--induced by the process of freeway driving. The repetitious nature of that form of driving compared to a country road would differentiate a theta state and a beta state in order to perform the driving task safely.
Individuals who do a lot of freeway driving often get good ideas during those periods when they are in theta. Individuals who run outdoors often are in the state of mental relaxation that is slower than alpha and when in theta, they are prone to a flow of ideas. This can also occur in the shower or tub or even while shaving or brushing your hair. It is a state where tasks become so automatic that you can mentally disengage from them. The ideation that can take place during the theta state is often free flow and occurs without censorship or guilt. It is typically a very positive mental state.
The final brainwave state is delta. Here the brainwaves are of the greatest amplitude and slowest frequency. They typically center around a range of 1.5 to 4 cycles per second. They never go down to zero because that would mean that you were brain dead. But, deep dreamless sleep would take you down to the lowest frequency. Typically, 2 to 3 cycles a second.
When we go to bed and read for a few minutes before attempting sleep, we are likely to be in low beta. When we put the book down, turn off the lights and close our eyes, our brainwaves will descend from beta, to alpha, to theta and finally, when we fall asleep, to delta.
It is a well known fact that humans dream in 90 minute cycles. When the delta brainwave frequencies increase into the frequency of theta brainwaves, active dreaming takes place and often becomes more experiential to the person. Typically, when this occurs there is rapid eye movement, which is characteristic of active dreaming. This is called REM, and is a well known phenomenon.
When an individual awakes from a deep sleep in preparation for getting up, their brainwave frequencies will increase through the different specific stages of brainwave activity. That is, they will increase from delta to theta and then to alpha and finally, when the alarm goes off, into beta. If that individual hits the snooze alarm button they will drop in frequency to a non-aroused state, or even into theta, or sometimes fall back to sleep in delta. During this awakening cycle it is possible for individuals to stay in the theta state for an extended period of say, five to 15 minutes--which would allow them to have a free flow of ideas about yesterday's events or to contemplate the activities of the forthcoming day. This time can be an extremely productive and can be a period of very meaningful and creative mental activity.
In summary, there are four brainwave states that range from the high amplitude, low frequency delta to the low amplitude, high frequency beta. These brainwave states range from deep dreamless sleep to high arousal. The same four brainwave states are common to the human species. Men, women and children of all ages experience the same characteristic brainwaves. They are consistent across cultures and country boundaries.
Research has shown that although one brainwave state may predominate at any given time, depending on the activity level of the individual, the remaining three brain states are present in the mix of brainwaves at all times. In other words, while somebody is an aroused state and exhibiting a beta brainwave pattern, there also exists in that person's brain a component of alpha, theta and delta, even though these may be present only at the trace level.
It has been my personal experience that knowledge of brainwave states enhances a person's ability to make use of the specialized characteristics of those states: these include being mentally productive across a wide range of activities, such as being intensely focused, relaxed, creative and in restful sleep.
Even though this electrical power is very limited, it does occur in very specific ways that are characteristic of the human brain. Electrical activity emanating from the brain is displayed in the form of brainwaves. There are four categories of these brainwaves, ranging from the most activity to the least activity. When the brain is aroused and actively engaged in mental activities, it generates beta waves. These beta waves are of relatively low amplitude, and are the fastest of the four different brainwaves. The frequency of beta waves ranges from 15 to 40 cycles a second. Beta waves are characteristics of a strongly engaged mind. A person in active conversation would be in beta. A debater would be in high beta. A person making a speech, or a teacher, or a talk show host would all be in beta when they are engaged in their work.
The Brainwaves
The next brainwave category in order of frequency is alpha. Where beta represented arousal, alpha represents non-arousal. Alpha brainwaves are slower, and higher in amplitude. Their frequency ranges from 9 to 14 cycles per second. A person who has completed a task and sits down to rest is often in an alpha state. A person who takes time out to reflect or meditate is usually in an alpha state. A person who takes a break from a conference and walks in the garden is often in an alpha state.
The next state, theta brainwaves, are typically of even greater amplitude and slower frequency. This frequency range is normally between 5 and 8 cycles a second. A person who has taken time off from a task and begins to daydream is often in a theta brainwave state. A person who is driving on a freeway, and discovers that they can't recall the last five miles, is often in a theta state--induced by the process of freeway driving. The repetitious nature of that form of driving compared to a country road would differentiate a theta state and a beta state in order to perform the driving task safely.
Individuals who do a lot of freeway driving often get good ideas during those periods when they are in theta. Individuals who run outdoors often are in the state of mental relaxation that is slower than alpha and when in theta, they are prone to a flow of ideas. This can also occur in the shower or tub or even while shaving or brushing your hair. It is a state where tasks become so automatic that you can mentally disengage from them. The ideation that can take place during the theta state is often free flow and occurs without censorship or guilt. It is typically a very positive mental state.
The final brainwave state is delta. Here the brainwaves are of the greatest amplitude and slowest frequency. They typically center around a range of 1.5 to 4 cycles per second. They never go down to zero because that would mean that you were brain dead. But, deep dreamless sleep would take you down to the lowest frequency. Typically, 2 to 3 cycles a second.
When we go to bed and read for a few minutes before attempting sleep, we are likely to be in low beta. When we put the book down, turn off the lights and close our eyes, our brainwaves will descend from beta, to alpha, to theta and finally, when we fall asleep, to delta.
It is a well known fact that humans dream in 90 minute cycles. When the delta brainwave frequencies increase into the frequency of theta brainwaves, active dreaming takes place and often becomes more experiential to the person. Typically, when this occurs there is rapid eye movement, which is characteristic of active dreaming. This is called REM, and is a well known phenomenon.
When an individual awakes from a deep sleep in preparation for getting up, their brainwave frequencies will increase through the different specific stages of brainwave activity. That is, they will increase from delta to theta and then to alpha and finally, when the alarm goes off, into beta. If that individual hits the snooze alarm button they will drop in frequency to a non-aroused state, or even into theta, or sometimes fall back to sleep in delta. During this awakening cycle it is possible for individuals to stay in the theta state for an extended period of say, five to 15 minutes--which would allow them to have a free flow of ideas about yesterday's events or to contemplate the activities of the forthcoming day. This time can be an extremely productive and can be a period of very meaningful and creative mental activity.
In summary, there are four brainwave states that range from the high amplitude, low frequency delta to the low amplitude, high frequency beta. These brainwave states range from deep dreamless sleep to high arousal. The same four brainwave states are common to the human species. Men, women and children of all ages experience the same characteristic brainwaves. They are consistent across cultures and country boundaries.
Research has shown that although one brainwave state may predominate at any given time, depending on the activity level of the individual, the remaining three brain states are present in the mix of brainwaves at all times. In other words, while somebody is an aroused state and exhibiting a beta brainwave pattern, there also exists in that person's brain a component of alpha, theta and delta, even though these may be present only at the trace level.
It has been my personal experience that knowledge of brainwave states enhances a person's ability to make use of the specialized characteristics of those states: these include being mentally productive across a wide range of activities, such as being intensely focused, relaxed, creative and in restful sleep.
somatic mtDNA mutations with adult onset leukaemia
Mitochondria, the power house of the cell are under the control of genomic DNA (mtDNA) and nuclear DNA.The mtDNA is a 16.6 kb molecule, encodes 13 subunits of respiratory chain complexes, as well as 22 tRNA and two ribosomal RNA for intramitochondrial synthesis. Mutations in mitochondrial DNA (mtDNA) are frequent in cancers but it is not yet clearly established whether they are modifier events involved in cancer progression or whether they are a consequence of tumorigenesis. We therefore decided to determine the spectrum of somatic mtDNA mutation in adult-onset leukaemia by comparing directly the entire mitochondrial genome sequence from normal and leukemic cells obtained from 24 patients with both chronic and acute presentations. This comparison gives the change in nucleotide composition. On this basis we can repair those sequences and modify it by gene therapy. By doing this the problems of graft rejection and bone marrow replacement are solved and the disease leukaemia can be treated in a more efficient way.
Introduction: Mitochondria are structures within cells that convert the energy from food into a form that cells can use. Although most DNA is packaged in chromosomes within the nucleus, mitochondria also have a small amount of their own DNA. This genetic material is known as mitochondrial DNA or mtDNA. In humans, mitochondrial DNA spans about 16,500 DNA building blocks (base pairs), representing a fraction of the total DNA in cells.
Mitochondrial DNA contains 37 genes, all of which are essential for normal mitochondrial function. Thirteen of these genes provide instructions for making enzymes involved in oxidative phosphorylation. Oxidative phosphorylation is a process that uses oxygen and simple sugars to create adenosine triphosphate (ATP), the cell's main energy source. The remaining genes provide instructions for making molecules called transfer RNAs (tRNAs) and ribosomal RNAs (rRNAs), which are chemical cousins of DNA. These types of RNA help assemble protein building blocks (amino acids) into functioning proteins.
Genes
ATP synthase: MT-ATP6, MT-ATP8
cytochrome c oxidase: MT-CO1, MT-CO2, MT-CO3, MT-CYB
NADH dehydrogenase: MT-ND1, MT-ND2, MT-ND3, MT-ND4, MT-ND4L, MT-ND5, MT-ND6
12S, 16S: MT-RNR1, MT-RNR2
tRNA: MT-TA, MT-TC, MT-TD, MT-TE, MT-TF, MT-TG, MT-TH, MT-TI, MT-TK, MT-TL1, MT-TL2, MT-TM, MT-TN, MT-TP, MT-TQ, MT-TR, MT-TS1, MT-TS2, MT-TT, MT-TV, MT-TW, MT-TY, MT1X
Mitochondrial DNA is prone to noninherited (somatic) mutations. Somatic mutations occur in the DNA of certain cells during a person’s lifetime and typically are not passed to future generations. Somatic mutations in mitochondrial DNA have been reported in some forms of cancer, including breast, colon, stomach, liver, and kidney tumours. These mutations also have been associated with cancer of blood-forming tissue (leukaemia) and cancer of immune system cells (lymphoma).
Somatic mutations in mitochondrial DNA may increase the production of potentially harmful molecules called reactive oxygen species. Mitochondrial DNA is particularly vulnerable to the effects of these molecules and has a limited ability to repair itself. As a result, reactive oxygen species easily damage mitochondrial DNA, causing a buildup of additional somatic mutations. Researchers continue to investigate how these mutations may lead to uncontrolled cell division and the growth of cancerous tumours.
The mtDNA is inherited from mother’s body. In case of sperm the maximum mtDNA stays in the tail which is isolated during fertilization. As a result the zygote gets only maternal mtDNA and no paternal DNA.
Materials and methods
Patients
24 adult patients (aged 18–88 years), six with acute lymphatic leukaemia (ALL), six with acute myeloid leukaemia (AML), six with chronic lymphatic leukaemia (CLL) and six with chronic myeloid leukaemia (CML) had been studied. All had been given their informed consent for these investigations, which were approved by the local Ethics Committee. Tumour samples were represented by bone marrow (ALL and AML), blood with high white blood cell count (CLL) or blood during therapy failure (CML). For each patient, buccal epithelial cells were collected from mouthwashes by centrifugation as representative of normal tissue.
mtDNA sequencing
DNA was extracted by standard procedures and the entire mitochondrial genome was amplified in 28 overlapping fragments of between 600 and 700 bp using M13-tagged oligodeoxynucleotide primers to facilitate the direct sequencing of the PCR-amplified products. A complete list of the primer pairs and sequencing protocol has been published previously.26 Briefly, following PCR amplification, samples were purified to remove unincorporated primers and sequenced directly using BigDye terminator cycle sequencing chemistries (PE Biosystems) on an ABI 377 automated DNA sequencer. The sequences obtained were compared directly to the revised Cambridge reference sequence (rCRS)27 using Sequence Navigator and Factura software (PE Biosystems) to identify sequence variants. Somatic mutations were identified by directly comparing the sequence differences detected in buccal and tumour samples from individual patients.
Introduction: Mitochondria are structures within cells that convert the energy from food into a form that cells can use. Although most DNA is packaged in chromosomes within the nucleus, mitochondria also have a small amount of their own DNA. This genetic material is known as mitochondrial DNA or mtDNA. In humans, mitochondrial DNA spans about 16,500 DNA building blocks (base pairs), representing a fraction of the total DNA in cells.
Mitochondrial DNA contains 37 genes, all of which are essential for normal mitochondrial function. Thirteen of these genes provide instructions for making enzymes involved in oxidative phosphorylation. Oxidative phosphorylation is a process that uses oxygen and simple sugars to create adenosine triphosphate (ATP), the cell's main energy source. The remaining genes provide instructions for making molecules called transfer RNAs (tRNAs) and ribosomal RNAs (rRNAs), which are chemical cousins of DNA. These types of RNA help assemble protein building blocks (amino acids) into functioning proteins.
Genes
ATP synthase: MT-ATP6, MT-ATP8
cytochrome c oxidase: MT-CO1, MT-CO2, MT-CO3, MT-CYB
NADH dehydrogenase: MT-ND1, MT-ND2, MT-ND3, MT-ND4, MT-ND4L, MT-ND5, MT-ND6
12S, 16S: MT-RNR1, MT-RNR2
tRNA: MT-TA, MT-TC, MT-TD, MT-TE, MT-TF, MT-TG, MT-TH, MT-TI, MT-TK, MT-TL1, MT-TL2, MT-TM, MT-TN, MT-TP, MT-TQ, MT-TR, MT-TS1, MT-TS2, MT-TT, MT-TV, MT-TW, MT-TY, MT1X
Mitochondrial DNA is prone to noninherited (somatic) mutations. Somatic mutations occur in the DNA of certain cells during a person’s lifetime and typically are not passed to future generations. Somatic mutations in mitochondrial DNA have been reported in some forms of cancer, including breast, colon, stomach, liver, and kidney tumours. These mutations also have been associated with cancer of blood-forming tissue (leukaemia) and cancer of immune system cells (lymphoma).
Somatic mutations in mitochondrial DNA may increase the production of potentially harmful molecules called reactive oxygen species. Mitochondrial DNA is particularly vulnerable to the effects of these molecules and has a limited ability to repair itself. As a result, reactive oxygen species easily damage mitochondrial DNA, causing a buildup of additional somatic mutations. Researchers continue to investigate how these mutations may lead to uncontrolled cell division and the growth of cancerous tumours.
The mtDNA is inherited from mother’s body. In case of sperm the maximum mtDNA stays in the tail which is isolated during fertilization. As a result the zygote gets only maternal mtDNA and no paternal DNA.
Materials and methods
Patients
24 adult patients (aged 18–88 years), six with acute lymphatic leukaemia (ALL), six with acute myeloid leukaemia (AML), six with chronic lymphatic leukaemia (CLL) and six with chronic myeloid leukaemia (CML) had been studied. All had been given their informed consent for these investigations, which were approved by the local Ethics Committee. Tumour samples were represented by bone marrow (ALL and AML), blood with high white blood cell count (CLL) or blood during therapy failure (CML). For each patient, buccal epithelial cells were collected from mouthwashes by centrifugation as representative of normal tissue.
mtDNA sequencing
DNA was extracted by standard procedures and the entire mitochondrial genome was amplified in 28 overlapping fragments of between 600 and 700 bp using M13-tagged oligodeoxynucleotide primers to facilitate the direct sequencing of the PCR-amplified products. A complete list of the primer pairs and sequencing protocol has been published previously.26 Briefly, following PCR amplification, samples were purified to remove unincorporated primers and sequenced directly using BigDye terminator cycle sequencing chemistries (PE Biosystems) on an ABI 377 automated DNA sequencer. The sequences obtained were compared directly to the revised Cambridge reference sequence (rCRS)27 using Sequence Navigator and Factura software (PE Biosystems) to identify sequence variants. Somatic mutations were identified by directly comparing the sequence differences detected in buccal and tumour samples from individual patients.
immunosuppressant drugs
PURPOSE. To determine alterations in expression of genes in herpes simples virus (HSV)-1 latently infected mouse trigeminal ganglia (TGs), after treatment with cyclophosphamide and dexamethasone.
METHODS. Scarified corneas of female BALB/c mice were inoculated with HSV-1 strain McKrae. Four weeks after inoculation, cyclophosphamide and dexamethasone were intravenously injected to induce HSV-1 reactivation. Uninfected mice were also treated with the immunosuppressants. Four groups of animals were studied: uninfected, not treated; uninfected, drug treated; latently infected, not treated; and latently infected, drug treated. PolyA+ mRNA from the TGs of each group was reverse transcribed, labeled with 32P, incubated on a 1185-gene array membrane, and analyzed by phosphorimaging. As a comparison and to confirm microarray results, semiquantitative RT-PCR was also performed for selected genes.
RESULTS. The immunosuppressive drugs significantly increased expression of two genes (calpactin 1 light chain and guanine nucleotide-binding protein –stimulating polypeptide [GNAS]) in the ganglia of uninfected mice compared with those in untreated uninfected mice. Ten genes were shown to be significantly increased in the latent TGs of mice treated with immunosuppressants compared with latently infected untreated mice. These genes were prostaglandin E2 receptor EP4 subtype (PTGER4), insulin promoter factor 1 (IPF1), glutathione S-transferase µ2, cyclin D2, peripherin, plasma glutathione peroxidase, methyl CpG-binding protein 2, retinal S-antigen, ErbB2 proto-oncogene, and GNAS. Eight genes were shown to be significantly decreased in the HSV-1 latent TGs treated with the drugs, compared with untreated latently infected mice. These genes were peripheral myelin protein 22, decorin, transcription factor AP-1, dystroglycan 1, myelin protein zero, mitogen-activated protein kinase 3, prothymosin beta 4, and brain lipid-binding protein. The results obtained by semiquantitative RT-PCR were similar to those obtained by microarray analysis.
CONCLUSIONS. Those genes with expression altered by immunosuppressive drug treatment may play an important role in ocular HSV-1 recurrence. Changes in expression of genes in the prostaglandin pathway, a transcription factor, and an enzyme in the cell cycle are considered especially important in HSV-1 reactivation by immunosuppression and are reviewed.
METHODS. Scarified corneas of female BALB/c mice were inoculated with HSV-1 strain McKrae. Four weeks after inoculation, cyclophosphamide and dexamethasone were intravenously injected to induce HSV-1 reactivation. Uninfected mice were also treated with the immunosuppressants. Four groups of animals were studied: uninfected, not treated; uninfected, drug treated; latently infected, not treated; and latently infected, drug treated. PolyA+ mRNA from the TGs of each group was reverse transcribed, labeled with 32P, incubated on a 1185-gene array membrane, and analyzed by phosphorimaging. As a comparison and to confirm microarray results, semiquantitative RT-PCR was also performed for selected genes.
RESULTS. The immunosuppressive drugs significantly increased expression of two genes (calpactin 1 light chain and guanine nucleotide-binding protein –stimulating polypeptide [GNAS]) in the ganglia of uninfected mice compared with those in untreated uninfected mice. Ten genes were shown to be significantly increased in the latent TGs of mice treated with immunosuppressants compared with latently infected untreated mice. These genes were prostaglandin E2 receptor EP4 subtype (PTGER4), insulin promoter factor 1 (IPF1), glutathione S-transferase µ2, cyclin D2, peripherin, plasma glutathione peroxidase, methyl CpG-binding protein 2, retinal S-antigen, ErbB2 proto-oncogene, and GNAS. Eight genes were shown to be significantly decreased in the HSV-1 latent TGs treated with the drugs, compared with untreated latently infected mice. These genes were peripheral myelin protein 22, decorin, transcription factor AP-1, dystroglycan 1, myelin protein zero, mitogen-activated protein kinase 3, prothymosin beta 4, and brain lipid-binding protein. The results obtained by semiquantitative RT-PCR were similar to those obtained by microarray analysis.
CONCLUSIONS. Those genes with expression altered by immunosuppressive drug treatment may play an important role in ocular HSV-1 recurrence. Changes in expression of genes in the prostaglandin pathway, a transcription factor, and an enzyme in the cell cycle are considered especially important in HSV-1 reactivation by immunosuppression and are reviewed.
Sunday, October 19, 2008
human gene affects memory
NIH scientists have shown that a common gene variant influences memory for events in humans by altering a growth factor in the brain's memory hub. On average, people with a particular version of the gene that codes for brain derived neurotrophic factor (BDNF) performed worse on tests of episodic memory — tasks like recalling what happened yesterday. They also showed differences in activation of the hippocampus, a brain area known to mediate memory, and signs of decreased neuronal health and interconnections. These effects are likely traceable to limited movement and secretion of BDNF within cells, according to the study, which reveals how a gene affects the normal range of human memory, and confirms that BDNF affects human hippocampal function much as it does animals'.
Michael Egan, M.D., Daniel Weinberger, M.D., National Institute of Mental Health (NIMH), Bai Lu, Ph.D., National Institute of Child Health and Human Development (NICHD) and colleagues, report on their discovery in the January 24 issue of Cell.
Long known to be critical for the growth and survival of neurons, BDNF has also recently been shown to play a key role in memory and hippocampal function in animals. To find out if it works similarly in humans, the researchers explored the consequences of a tiny variance in the human BDNF gene, where its molecular makeup differs slightly across individuals. People inherit two copies of the BDNF gene — one from each parent — in either of two versions. Slightly more than a third inherit at least one copy of a version nicknamed "met," which the researchers have now linked to poorer memory. It's called "met" because its chemical sequence contains the amino acid methionine in a location where the more common version, "val," contains valine.
"We are finding that this one amino acid substitution exerts a substantial influence on human memory, presumably because of its effects on the biology of the hippocampus," said Weinberger.
Despite its negative effect on memory, the "met" version's survival in the human genome suggests that it "may confer some compensatory advantage in other biological processes," note the researchers. Although they found that it does not confer increased susceptibility to schizophrenia, they suggest that the "met" variant might contribute to risk for — or increase functional impairment in — other disorders involving hippocampal dysfunction, such as Alzheimer's disease or mood disorders.
Drawing on participants in the NIMH intramural sibling study of schizophrenia, Egan and colleagues first assessed their hippocampal function and related it to their BDNF gene types.
Among 641 normal controls, schizophrenia patients, and their unaffected siblings, those who had inherited two copies of the "met" variant scored significantly lower than their matched peers on tests of verbal episodic (event) memory. Most notably, normal controls with two copies of "met" scored 40 percent on delayed recall, compared to 70 percent for those with two copies of "val." BDNF gene type had no significant effect on tests of other types of memory, such as semantic or working memory.
The researchers then measured brain activity in two separate groups of healthy subjects while they were performing a working memory task that normally turns off hippocampus activity. Functional magnetic resonance imaging (fMRI) scans revealed that those with one copy of "met" showed a pattern of activation along the sides of the hippocampus, in contrast to lack of activation among those with two copies of "val."
Next, an MRI scanner was used to measure levels of a marker inside neurons indicating the cell's health and abundance of synapses — tiny junctions through which neurons communicate with each other. Again, subjects with one copy of "met" had lower levels of the marker, N-acetyl-aspartate (NAA), than matched individuals with two copies of "val." Analysis showed that NAA levels dropped as the number of inherited "met" variants increased, suggesting a possible "dose effect."
Unlike other growth factors, hippocampal BDNF is secreted, in part, in response to neuronal activity, making it a likely candidate for a key role in synaptic plasticity, learning and memory. To explore possible mechanisms underlying the observed "met"- related memory effect, the researchers examined the distribution, processing and secretion of the BDNF proteins expressed by the two different gene variants within hippocampal cells. When they tagged the gene variants with green fluorescent protein and introduced them into cultured neurons, they discovered that "val" BDNF spreads throughout the cell and into the branch-like dendrites that form synapses, while "met" BDNF mostly clumps inside the cell body without being transported to the synapses. To regulate memory function, BDNF must be secreted near the synapses.
"We were surprised to see that 'met' BDNF secretion can't be properly regulated by neural activity," said Lu.
The observed memory decrements are likely traceable to the failure of "met" BDNF to reach the synapses, as well as its inability to secrete in response to neuronal activity, say the researchers.
"Our study provides direct in vivo data that the molecular mechanisms related to activity dependent BDNF secretion and signaling, such as synaptic plasticity, may underlie humans' greatly expanded verbally-mediated memory system, just as it does for more rudimentary forms of memory in animals," said Egan.
In following-up their leads, the researchers are searching for a possible BDNF connection with the memory problems and hippocampal changes of Alzheimer's disease, depression and normal aging.
Also participating in the study were: Drs. Joseph Callicott, Terry Goldberg, Bhaskar Kolachana, Alessandro Bertolino, NIMH; Drs. Masami Kojima, Eugene Zaitsev, NICHD; Dr. David Goldman, National Institute on Alcohol Abuse and Alcoholism (NIAAA); Drs. Bert Gold, Michael Dean, National Cancer Institute (NCI).
NIMH, NICHD, NIAAA and NCI are part of the National Institutes of Health (NIH), the Federal Government's primary agency for biomedical and behavioral research. NIH is a component of the U.S. Department of Health and Human Services.
Graph shows the effect of BDNF gene type on performance during a test of delayed recall of memory for events among 641 participants in the NIMH Clinical Brain Disorders Branch sibling study of schizophrenia. Normal controls (heavy black line) who had inherited two copies of "met" scored 40 percent, compared to 70 percent for those with two copies of "val." Source: NIMH Clinical Brain Disorders Branch
Michael Egan, M.D., Daniel Weinberger, M.D., National Institute of Mental Health (NIMH), Bai Lu, Ph.D., National Institute of Child Health and Human Development (NICHD) and colleagues, report on their discovery in the January 24 issue of Cell.
Long known to be critical for the growth and survival of neurons, BDNF has also recently been shown to play a key role in memory and hippocampal function in animals. To find out if it works similarly in humans, the researchers explored the consequences of a tiny variance in the human BDNF gene, where its molecular makeup differs slightly across individuals. People inherit two copies of the BDNF gene — one from each parent — in either of two versions. Slightly more than a third inherit at least one copy of a version nicknamed "met," which the researchers have now linked to poorer memory. It's called "met" because its chemical sequence contains the amino acid methionine in a location where the more common version, "val," contains valine.
"We are finding that this one amino acid substitution exerts a substantial influence on human memory, presumably because of its effects on the biology of the hippocampus," said Weinberger.
Despite its negative effect on memory, the "met" version's survival in the human genome suggests that it "may confer some compensatory advantage in other biological processes," note the researchers. Although they found that it does not confer increased susceptibility to schizophrenia, they suggest that the "met" variant might contribute to risk for — or increase functional impairment in — other disorders involving hippocampal dysfunction, such as Alzheimer's disease or mood disorders.
Drawing on participants in the NIMH intramural sibling study of schizophrenia, Egan and colleagues first assessed their hippocampal function and related it to their BDNF gene types.
Among 641 normal controls, schizophrenia patients, and their unaffected siblings, those who had inherited two copies of the "met" variant scored significantly lower than their matched peers on tests of verbal episodic (event) memory. Most notably, normal controls with two copies of "met" scored 40 percent on delayed recall, compared to 70 percent for those with two copies of "val." BDNF gene type had no significant effect on tests of other types of memory, such as semantic or working memory.
The researchers then measured brain activity in two separate groups of healthy subjects while they were performing a working memory task that normally turns off hippocampus activity. Functional magnetic resonance imaging (fMRI) scans revealed that those with one copy of "met" showed a pattern of activation along the sides of the hippocampus, in contrast to lack of activation among those with two copies of "val."
Next, an MRI scanner was used to measure levels of a marker inside neurons indicating the cell's health and abundance of synapses — tiny junctions through which neurons communicate with each other. Again, subjects with one copy of "met" had lower levels of the marker, N-acetyl-aspartate (NAA), than matched individuals with two copies of "val." Analysis showed that NAA levels dropped as the number of inherited "met" variants increased, suggesting a possible "dose effect."
Unlike other growth factors, hippocampal BDNF is secreted, in part, in response to neuronal activity, making it a likely candidate for a key role in synaptic plasticity, learning and memory. To explore possible mechanisms underlying the observed "met"- related memory effect, the researchers examined the distribution, processing and secretion of the BDNF proteins expressed by the two different gene variants within hippocampal cells. When they tagged the gene variants with green fluorescent protein and introduced them into cultured neurons, they discovered that "val" BDNF spreads throughout the cell and into the branch-like dendrites that form synapses, while "met" BDNF mostly clumps inside the cell body without being transported to the synapses. To regulate memory function, BDNF must be secreted near the synapses.
"We were surprised to see that 'met' BDNF secretion can't be properly regulated by neural activity," said Lu.
The observed memory decrements are likely traceable to the failure of "met" BDNF to reach the synapses, as well as its inability to secrete in response to neuronal activity, say the researchers.
"Our study provides direct in vivo data that the molecular mechanisms related to activity dependent BDNF secretion and signaling, such as synaptic plasticity, may underlie humans' greatly expanded verbally-mediated memory system, just as it does for more rudimentary forms of memory in animals," said Egan.
In following-up their leads, the researchers are searching for a possible BDNF connection with the memory problems and hippocampal changes of Alzheimer's disease, depression and normal aging.
Also participating in the study were: Drs. Joseph Callicott, Terry Goldberg, Bhaskar Kolachana, Alessandro Bertolino, NIMH; Drs. Masami Kojima, Eugene Zaitsev, NICHD; Dr. David Goldman, National Institute on Alcohol Abuse and Alcoholism (NIAAA); Drs. Bert Gold, Michael Dean, National Cancer Institute (NCI).
NIMH, NICHD, NIAAA and NCI are part of the National Institutes of Health (NIH), the Federal Government's primary agency for biomedical and behavioral research. NIH is a component of the U.S. Department of Health and Human Services.
Graph shows the effect of BDNF gene type on performance during a test of delayed recall of memory for events among 641 participants in the NIMH Clinical Brain Disorders Branch sibling study of schizophrenia. Normal controls (heavy black line) who had inherited two copies of "met" scored 40 percent, compared to 70 percent for those with two copies of "val." Source: NIMH Clinical Brain Disorders Branch
brain activity during meditation
One basic concept of biology suggests that eukaryotic organelles arose after a primitive eukaryotic cell engulfed (swallowed, invaginated) a prokaryotic cell. This is called the endosymbiotic theory. After this invagination event, the concept continues, duplicate functions already possessed by the eukaryotic cell were eliminated, and only those prokaryotic functions that were advantageous to the eukaryotic cell were maintained. In particular, energy transduction functions, such as ATP and NADPH production, were maintained.
The two organelles that arose were the mitochondria, found in all eukoryotic cells, and chloroplasts which are found in plants and algae. Some of the genetic information of the prokaryotic cell was transferred to the nucleus of the eukaryotic cell. Chloroplast and mitochondrial sequences have been found in the nucleus of plant cells. Furthermore, chloroplast sequences have been found in the mitochondrial of plant cells. This is clear evidence that genetic control of certain biochemical functions was relinquished (or taken from) the progenitor cells. The following diagram shows the flow of genetic information from organelles in a plant cell.
It is important to note that all the basic functions of the Central Dogma of Molecular Genetics are found in organelles. This functions include DNA replication, RNA transcription and protein translation. Thus, certain gene products will result from the expression of the organelle DNA. The number of protein products from mitochondrial transcription is limited. One set of genes that are expressed are the rRNAs and tRNAs that are required for translation. Five known gene products are produced from the mammalian mitochondrial genome. These include subunits I, II and III for cytochrome oxidase, the apoprotein for cytochrome b and subunit 6 of the mitochondrial ATPase. In addition to these gene products, six ORFs have been identified. (ORF represents Open Reading Frame.) These are sequences that have transcription start and stop signals that bracket sequences that could produce a protein product, but the actual function of the product is not known. Finally, as we saw above the expression of organelle genes has a unique effect on the inheritance of certain traits.
This transfer of genetic information during the evolution of eukaryotic cells has also required the development of cooperative gene expression systems between the organelle and the nucleus. Cytochrome oxidase is one of the mitochondrial enzymes involved in ATP generation. As stated above subunits I, II, and III are encoded in the mitochondria. The remainder of the subunits of this seven subunit protein are encoded in the nucleus. The best studied example of coupled nuclear DNA/chloroplast DNA gene expression is for the protein RUBISCO (ribulose bisphoshpate carboxylase oxygenase). This is the enzyme that begins the fixation of atmospheric CO2 into sugar molecules. This enzyme has 16 subunits, eight large subunits and 8 small subunits. The large subunits are encoded by the chloroplast DNA whereas, the small subunits are encoded by nuclear DNA. Thus, for those proteins that are encoded by genes in two different cellular locations, gene expression has to be coordinated between the two locations for proper protein functioning.
Chloroplast Genomes
The chloroplast genomes of plants exhibit a far greater conversation of structure than plant mitochondrial genomes. These genomes are circular and the size of higher plant chloroplast DNAs are either *150 kb (for example, spinach) or *120 (for example pea). The difference in size can be accounted for by a deletion from the larger genome to generate the smaller. The gene order among all higher plant chloroplast genomes is essentially conserved.
As you would predict, many of chloroplast DNA genes encode proteins that are involved in photosynthesis. In total, the genome appears to encode for a complete set of rRNA and tRNA genes and *45 protein products. There are some differences between species, but these differences primarily are between higher plants and algae, which also contain chloroplast DNA.
RFLP proof that chloroplast DNA can be maternally inherited
As has been stated previously, to demonstrate that a trait is maternally inherited specific crosses need to be made to generate the required offspring. A number of crosses where made between cultivated tomato (L. esculentum) and a number of wild species. As we discussed previously, chloroplast DNA is a circular molecule *150 kb in size. Digestion of this molecule produces relatively few fragments. Within the plant cell, chloroplast DNA represents a significant portion (*15%) of the DNA. This is a result of the large number of chloroplasts per cell (*50) and the large number of chloroplast DNA molecules per chloroplast (*150).
Chloroplast DNA was obtained from F1 plants of a number of crosses in which L. esculentum was the female in the cross. As can be seen below, in each case the F1 restriction fragment pattern was identical to L. esculentum (sample 8). This is conclusive evidence that chloroplast DNA is inherited in a maternal manner. [The figures shown below are from Palmer and Zamir (1982) Proceedings of the National Academy of Science USA 79:5006.]
Mitochondrial Genomes
All of the eukaryotic species that have been analyzed to date have DNA in the mitochondria. But the size of this mitochondrial genome varies.
Size of Mitochondrial G enomes
Species |Size (kb)
--------------------------
Human | 16
Drosophila | 18
Yeast | 75
Turnip | 218
Corn | 570
Muskmelon | 2000
--------------------------
All of the mitochondrial genomes are circular. Even though there is a large size discrepancy between different species, especially between plants and animals, the number of genes that are expressed in each species is nearly the same, about 20. Thus the extra DNA that is found in the larger genomes does not appear to be required. Studies have shown that much of this DNA is in fact repeated sequences.
RFLP proof that mitochondrial DNA can be maternally inherited
Experiments designed to show that mitochondrial DNA was maternally inherited were analogous to those which demonstrated that chloroplast DNA was maternally inherited. Mouse is the experimental organism used to demonstrate this principle here. Reciprocal crosses were made between the species Mus domesticus, common mouse, and the wild species Mus spretus. F1 progeny where then backcrossed, with one of the two species serving as females. The restriction enzyme HincII is diagnostic for the mitochondrial DNA of the two species. M. domesticus mt DNA contains five restriction sites for the enzyme that generates four fragments whereas M. spretus mt DNA contains eight restriction sites which generate seven fragments. Only two of the fragments are the same size and presumably contain the same sequence information.
The figure below depicts the results of the backcross experiments. [The figure is from Gyllenstein et al. (1985) Journal of Heredity 76:321.] As you can see the female contributes the mitochondrial genome. These experiments have been repeated in other species, such as human, and the female has been shown to contribute the mitochondrial genome
The two organelles that arose were the mitochondria, found in all eukoryotic cells, and chloroplasts which are found in plants and algae. Some of the genetic information of the prokaryotic cell was transferred to the nucleus of the eukaryotic cell. Chloroplast and mitochondrial sequences have been found in the nucleus of plant cells. Furthermore, chloroplast sequences have been found in the mitochondrial of plant cells. This is clear evidence that genetic control of certain biochemical functions was relinquished (or taken from) the progenitor cells. The following diagram shows the flow of genetic information from organelles in a plant cell.
It is important to note that all the basic functions of the Central Dogma of Molecular Genetics are found in organelles. This functions include DNA replication, RNA transcription and protein translation. Thus, certain gene products will result from the expression of the organelle DNA. The number of protein products from mitochondrial transcription is limited. One set of genes that are expressed are the rRNAs and tRNAs that are required for translation. Five known gene products are produced from the mammalian mitochondrial genome. These include subunits I, II and III for cytochrome oxidase, the apoprotein for cytochrome b and subunit 6 of the mitochondrial ATPase. In addition to these gene products, six ORFs have been identified. (ORF represents Open Reading Frame.) These are sequences that have transcription start and stop signals that bracket sequences that could produce a protein product, but the actual function of the product is not known. Finally, as we saw above the expression of organelle genes has a unique effect on the inheritance of certain traits.
This transfer of genetic information during the evolution of eukaryotic cells has also required the development of cooperative gene expression systems between the organelle and the nucleus. Cytochrome oxidase is one of the mitochondrial enzymes involved in ATP generation. As stated above subunits I, II, and III are encoded in the mitochondria. The remainder of the subunits of this seven subunit protein are encoded in the nucleus. The best studied example of coupled nuclear DNA/chloroplast DNA gene expression is for the protein RUBISCO (ribulose bisphoshpate carboxylase oxygenase). This is the enzyme that begins the fixation of atmospheric CO2 into sugar molecules. This enzyme has 16 subunits, eight large subunits and 8 small subunits. The large subunits are encoded by the chloroplast DNA whereas, the small subunits are encoded by nuclear DNA. Thus, for those proteins that are encoded by genes in two different cellular locations, gene expression has to be coordinated between the two locations for proper protein functioning.
Chloroplast Genomes
The chloroplast genomes of plants exhibit a far greater conversation of structure than plant mitochondrial genomes. These genomes are circular and the size of higher plant chloroplast DNAs are either *150 kb (for example, spinach) or *120 (for example pea). The difference in size can be accounted for by a deletion from the larger genome to generate the smaller. The gene order among all higher plant chloroplast genomes is essentially conserved.
As you would predict, many of chloroplast DNA genes encode proteins that are involved in photosynthesis. In total, the genome appears to encode for a complete set of rRNA and tRNA genes and *45 protein products. There are some differences between species, but these differences primarily are between higher plants and algae, which also contain chloroplast DNA.
RFLP proof that chloroplast DNA can be maternally inherited
As has been stated previously, to demonstrate that a trait is maternally inherited specific crosses need to be made to generate the required offspring. A number of crosses where made between cultivated tomato (L. esculentum) and a number of wild species. As we discussed previously, chloroplast DNA is a circular molecule *150 kb in size. Digestion of this molecule produces relatively few fragments. Within the plant cell, chloroplast DNA represents a significant portion (*15%) of the DNA. This is a result of the large number of chloroplasts per cell (*50) and the large number of chloroplast DNA molecules per chloroplast (*150).
Chloroplast DNA was obtained from F1 plants of a number of crosses in which L. esculentum was the female in the cross. As can be seen below, in each case the F1 restriction fragment pattern was identical to L. esculentum (sample 8). This is conclusive evidence that chloroplast DNA is inherited in a maternal manner. [The figures shown below are from Palmer and Zamir (1982) Proceedings of the National Academy of Science USA 79:5006.]
Mitochondrial Genomes
All of the eukaryotic species that have been analyzed to date have DNA in the mitochondria. But the size of this mitochondrial genome varies.
Size of Mitochondrial G enomes
Species |Size (kb)
--------------------------
Human | 16
Drosophila | 18
Yeast | 75
Turnip | 218
Corn | 570
Muskmelon | 2000
--------------------------
All of the mitochondrial genomes are circular. Even though there is a large size discrepancy between different species, especially between plants and animals, the number of genes that are expressed in each species is nearly the same, about 20. Thus the extra DNA that is found in the larger genomes does not appear to be required. Studies have shown that much of this DNA is in fact repeated sequences.
RFLP proof that mitochondrial DNA can be maternally inherited
Experiments designed to show that mitochondrial DNA was maternally inherited were analogous to those which demonstrated that chloroplast DNA was maternally inherited. Mouse is the experimental organism used to demonstrate this principle here. Reciprocal crosses were made between the species Mus domesticus, common mouse, and the wild species Mus spretus. F1 progeny where then backcrossed, with one of the two species serving as females. The restriction enzyme HincII is diagnostic for the mitochondrial DNA of the two species. M. domesticus mt DNA contains five restriction sites for the enzyme that generates four fragments whereas M. spretus mt DNA contains eight restriction sites which generate seven fragments. Only two of the fragments are the same size and presumably contain the same sequence information.
The figure below depicts the results of the backcross experiments. [The figure is from Gyllenstein et al. (1985) Journal of Heredity 76:321.] As you can see the female contributes the mitochondrial genome. These experiments have been repeated in other species, such as human, and the female has been shown to contribute the mitochondrial genome
mitochondtrial dna mutation in somatic cells
Mitochondrial DNA (mtDNA) is the DNA located in organelles called mitochondria. Most other DNA present in eukaryotic organisms is found in the cell nucleus. Nuclear and mitochondrial DNA are thought to be of separate evolutionary origin, with the mtDNA being derived from the circular genomes of the bacteria that were engulfed by the early ancestors of today's eukaryotic cells. Each mitochondrion is estimated to contain 2-10 mtDNA copies.[1] In the cells of extant organisms, the vast majority of the proteins present in the mitochondria (numbering approximately 1500 different types in mammals) are coded for by nuclear DNA, but the genes for some of them, if not most, are thought to have originally been of bacterial origin, having since been transferred to the eukaryotic nucleus during evolution. Among multicellular animals (metazoans), nearly all of the mtDNA in a fertilized egg (zygote) is inherited from only one parent - the female. One mechanism for this is simple dilution: an egg contains 100,000 to 1,000,000 mitochondria, whereas a sperm contains only 10 to 100. Another mechanism, documented for a few organisms, is that the sperm mitochondria do not enter the egg. Whatever the mechanism, this single parent (uniparental) pattern of mtDNA inheritance is found in most animals, most plants and in fungi as well.
In humans (and probably in metazoans in general), 100-10,000 separate copies of mtDNA are usually present per cell (egg and sperm cells are exceptions). In mammals, each circular mtDNA molecule consists of 15,000-17,000 base pairs, which encode the same 37 genes: 13 for proteins (polypeptides), 22 for transfer RNA (tRNA) and one each for the small and large subunits of ribosomal RNA (rRNA). This pattern is also seen among most metazoans, although in some cases one or more of the 37 genes is absent and the mtDNA size range is greater. Even greater variation in mtDNA gene content and size exists among fungi and plants, although there appears to be a core subset of genes that are present in all eukaryotes (except for the few that have no mitochondria at all). Some plant species have enormous mtDNAs (as many as 2,500,000 base pairs per mtDNA molecule!) but, surprisingly, even those huge mtDNAs contain the same number and kinds of genes as related plants with much smaller mtDNAs.Contents
1 Use in identification
2 Mitochondrial inheritance
2.1 Female inheritance
2.2 Male inheritance
3 Genes
4 Genetic influence
4.1 Genetic illness
5 See also
6 References
7 External links
Use in identification
Unlike nuclear DNA, which is inherited from both parents and in which genes are rearranged in the process of recombination, there is usually no change in mtDNA from parent to offspring. Although mtDNA also recombines, it does so with copies of itself within the same mitochondrion. Because of this and because the mutation rate of animal mtDNA is higher than that of nuclear DNA,[2] mtDNA is a powerful tool for tracking ancestry through females (matrilineage) and has been used in this role to track the ancestry of many species back hundreds of generations. Human mtDNA can be used to identify individuals.[3]
Because the base sequence of animal mtDNA changes rapidly, it is useful for assessing genetic relationships of individuals or groups within a species and also for identifying and quantifying the phylogeny (evolutionary relationships; see phylogenetics) among different species, provided they are not too distantly related. To do this, biologists determine and then compare the mtDNA sequences from different individuals or species. Data from the comparisons is used to construct a network of relationships among the sequences, which provides an estimate of the relationships among the individuals or species from which the mtDNAs were taken. This approach has limits that are imposed by the rate of mtDNA sequence change. In animals, the rapid rate of change makes mtDNA most useful for comparisons of individuals within species and for comparisons of species that are closely or moderately-closely related, among which the number of sequence differences can be easily counted. As the species become more distantly related, the number of sequence differences becomes very large; changes begin to accumulate on changes until an accurate count becomes impossible.
Mitochondrial inheritance
Female inheritance
In sexually reproducing organisms, mitochondria are normally inherited exclusively from the mother. The mitochondria in mammalian sperm are usually destroyed by the egg cell after fertilization. Also, most mitochondria are present at the base of the sperm's tail, which is used for propelling the sperm cells. Sometimes the tail is lost during fertilization. In 1999 it was reported that paternal sperm mitochondria (containing mtDNA) are marked with ubiquitin to select them for later destruction inside the embryo.[4] Some in vitro fertilization techniques, particularly injecting a sperm into an oocyte, may interfere with this.
The fact that mitochondrial DNA is maternally inherited enables researchers to trace maternal lineage far back in time. (Y chromosomal DNA, paternally inherited, is used in an analogous way to trace the agnate lineage.) This is accomplished in humans by sequencing one or more of the hypervariable control regions (HVR1 or HVR2) of the mitochondrial DNA. HVR1 consists of about 440 base pairs. These 440 base pairs are then compared to the control regions of other individuals (either specific people or subjects in a database) to determine maternal lineage. Most often, the comparison is made to the revised. Vilà et al have published studies tracing the matrilineal descent of domestic dogs to wolves.[5] The concept of the Mitochondrial Eve is based on the same type of analysis, attempting to discover the origin of humanity by tracking the lineage back in time.
Because mtDNA is not highly conserved and has a rapid mutation rate, it is useful for studying the evolutionary relationships - phylogeny - of organisms. Biologists can determine and then compare mtDNA sequences among different species and use the comparisons to build an evolutionary tree for the species examined.
Male inheritance
It has been reported that mitochondria can occasionally be inherited from the father in some species such as mussels.[6][7] Paternally inherited mitochondria have also been reported in some insects such as the fruit fly[8] and the honeybee.[9]
Evidence supports rare instances of male mitochondrial inheritance in some mammals as well. Specifically, documented occurrences exist for mice,[10][11] where the male-inherited mitochondria was subsequently rejected. It has also been found in sheep,[12] and in cloned cattle.[13] It has been found in a single case in a human male and was linked to infertility.[14]
While many of these cases involve cloned embryos or subsequent rejection of the paternal mitochondria, others document in vivo inheritance and persistence under lab conditions.
Genes
ATP synthase: MT-ATP6, MT-ATP8
cytochrome c oxidase: MT-CO1, MT-CO2, MT-CO3, MT-CYB
NADH dehydrogenase: MT-ND1, MT-ND2, MT-ND3, MT-ND4, MT-ND4L, MT-ND5, MT-ND6
12S, 16S: MT-RNR1, MT-RNR2
tRNA: MT-TA, MT-TC, MT-TD, MT-TE, MT-TF, MT-TG, MT-TH, MT-TI, MT-TK, MT-TL1, MT-TL2, MT-TM, MT-TN, MT-TP, MT-TQ, MT-TR, MT-TS1, MT-TS2, MT-TT, MT-TV, MT-TW, MT-TY, MT1X
Genetic influence
Genetic illness
Mutations of mitochondrial DNA can lead to a number of illnesses including exercise intolerance and Kearns-Sayre syndrome (KSS), which causes a person to lose full function of their heart, eye, and muscle movements. (See also Mitochondrial disease).
Mitochondrial disease
Human mitochondrial genetics
Paternal mtDNA transmission
Single origin theory
Mitochondrial Eve
Mitochondrial CRS
In humans (and probably in metazoans in general), 100-10,000 separate copies of mtDNA are usually present per cell (egg and sperm cells are exceptions). In mammals, each circular mtDNA molecule consists of 15,000-17,000 base pairs, which encode the same 37 genes: 13 for proteins (polypeptides), 22 for transfer RNA (tRNA) and one each for the small and large subunits of ribosomal RNA (rRNA). This pattern is also seen among most metazoans, although in some cases one or more of the 37 genes is absent and the mtDNA size range is greater. Even greater variation in mtDNA gene content and size exists among fungi and plants, although there appears to be a core subset of genes that are present in all eukaryotes (except for the few that have no mitochondria at all). Some plant species have enormous mtDNAs (as many as 2,500,000 base pairs per mtDNA molecule!) but, surprisingly, even those huge mtDNAs contain the same number and kinds of genes as related plants with much smaller mtDNAs.Contents
1 Use in identification
2 Mitochondrial inheritance
2.1 Female inheritance
2.2 Male inheritance
3 Genes
4 Genetic influence
4.1 Genetic illness
5 See also
6 References
7 External links
Use in identification
Unlike nuclear DNA, which is inherited from both parents and in which genes are rearranged in the process of recombination, there is usually no change in mtDNA from parent to offspring. Although mtDNA also recombines, it does so with copies of itself within the same mitochondrion. Because of this and because the mutation rate of animal mtDNA is higher than that of nuclear DNA,[2] mtDNA is a powerful tool for tracking ancestry through females (matrilineage) and has been used in this role to track the ancestry of many species back hundreds of generations. Human mtDNA can be used to identify individuals.[3]
Because the base sequence of animal mtDNA changes rapidly, it is useful for assessing genetic relationships of individuals or groups within a species and also for identifying and quantifying the phylogeny (evolutionary relationships; see phylogenetics) among different species, provided they are not too distantly related. To do this, biologists determine and then compare the mtDNA sequences from different individuals or species. Data from the comparisons is used to construct a network of relationships among the sequences, which provides an estimate of the relationships among the individuals or species from which the mtDNAs were taken. This approach has limits that are imposed by the rate of mtDNA sequence change. In animals, the rapid rate of change makes mtDNA most useful for comparisons of individuals within species and for comparisons of species that are closely or moderately-closely related, among which the number of sequence differences can be easily counted. As the species become more distantly related, the number of sequence differences becomes very large; changes begin to accumulate on changes until an accurate count becomes impossible.
Mitochondrial inheritance
Female inheritance
In sexually reproducing organisms, mitochondria are normally inherited exclusively from the mother. The mitochondria in mammalian sperm are usually destroyed by the egg cell after fertilization. Also, most mitochondria are present at the base of the sperm's tail, which is used for propelling the sperm cells. Sometimes the tail is lost during fertilization. In 1999 it was reported that paternal sperm mitochondria (containing mtDNA) are marked with ubiquitin to select them for later destruction inside the embryo.[4] Some in vitro fertilization techniques, particularly injecting a sperm into an oocyte, may interfere with this.
The fact that mitochondrial DNA is maternally inherited enables researchers to trace maternal lineage far back in time. (Y chromosomal DNA, paternally inherited, is used in an analogous way to trace the agnate lineage.) This is accomplished in humans by sequencing one or more of the hypervariable control regions (HVR1 or HVR2) of the mitochondrial DNA. HVR1 consists of about 440 base pairs. These 440 base pairs are then compared to the control regions of other individuals (either specific people or subjects in a database) to determine maternal lineage. Most often, the comparison is made to the revised. Vilà et al have published studies tracing the matrilineal descent of domestic dogs to wolves.[5] The concept of the Mitochondrial Eve is based on the same type of analysis, attempting to discover the origin of humanity by tracking the lineage back in time.
Because mtDNA is not highly conserved and has a rapid mutation rate, it is useful for studying the evolutionary relationships - phylogeny - of organisms. Biologists can determine and then compare mtDNA sequences among different species and use the comparisons to build an evolutionary tree for the species examined.
Male inheritance
It has been reported that mitochondria can occasionally be inherited from the father in some species such as mussels.[6][7] Paternally inherited mitochondria have also been reported in some insects such as the fruit fly[8] and the honeybee.[9]
Evidence supports rare instances of male mitochondrial inheritance in some mammals as well. Specifically, documented occurrences exist for mice,[10][11] where the male-inherited mitochondria was subsequently rejected. It has also been found in sheep,[12] and in cloned cattle.[13] It has been found in a single case in a human male and was linked to infertility.[14]
While many of these cases involve cloned embryos or subsequent rejection of the paternal mitochondria, others document in vivo inheritance and persistence under lab conditions.
Genes
ATP synthase: MT-ATP6, MT-ATP8
cytochrome c oxidase: MT-CO1, MT-CO2, MT-CO3, MT-CYB
NADH dehydrogenase: MT-ND1, MT-ND2, MT-ND3, MT-ND4, MT-ND4L, MT-ND5, MT-ND6
12S, 16S: MT-RNR1, MT-RNR2
tRNA: MT-TA, MT-TC, MT-TD, MT-TE, MT-TF, MT-TG, MT-TH, MT-TI, MT-TK, MT-TL1, MT-TL2, MT-TM, MT-TN, MT-TP, MT-TQ, MT-TR, MT-TS1, MT-TS2, MT-TT, MT-TV, MT-TW, MT-TY, MT1X
Genetic influence
Genetic illness
Mutations of mitochondrial DNA can lead to a number of illnesses including exercise intolerance and Kearns-Sayre syndrome (KSS), which causes a person to lose full function of their heart, eye, and muscle movements. (See also Mitochondrial disease).
Mitochondrial disease
Human mitochondrial genetics
Paternal mtDNA transmission
Single origin theory
Mitochondrial Eve
Mitochondrial CRS
to study the patterning of memory in human brain
Aim:
To study the patterning of memory in human brain
Theory:
The human brain has 4 lobes. The frontal lobe is for intellectual activity like learning, memorizing, emotion etc. It is not known perfectly how the memorizing process inside a brain takes place. The different lobes play a different role in the fore said process. In this study we try to examine which part of the brain is hyperactive during the learning process. The brain has capability to generate waves which can be detected by EEG. We try to locate a particular area of the brain and waves associated for learning and memorizing by a simple experiment described in the next section. More or less no literature backup is available to support the current study. Hence this paper will have preliminary result to study and localize the memory patterns in the human brain.
Experiment:
1. A suitable candidate is chosen.
2. He is given a paragraph from a unknown source to read and memorize.
3. In this process EEG electrodes are set up on the scalp of the subject and the associated waves generated from the various parts are studied.
4. A particular region in the brain which is the most hyperactive will be chosen and more trials will be done on that part alone and the corresponding EEG waves will be analyzed
Equipments:
EEG machine (available at BCI Centre, CSE dept)
Duration:
1 month
Estimated Budget:
NIL
Scope of the study:
It leads to a better understanding of human memory and a probability of storing data in human brain artificially. The human brain has 4 lobes. The frontal lobe is for intellectual activity like learning, memorizing, emotion etc. It is not known perfectly how the memorizing process inside a brain takes place. The different lobes play a different role in the fore said process. In this study we try to examine which part of the brain is hyperactive during the learning process. The brain has capability to generate waves which can be detected by EEG. We try to locate a particular area of the brain and waves associated for learning and memorizing by a simple experiment described in the next section. More or less no literature backup is available to support the current study. Hence this paper will have preliminary result to study and localize the memory patterns in the human brain.
Experiment:
1. A suitable candidate is chosen.
2. He is given a paragraph from a unknown source to read and memorize.
3. In this process EEG electrodes are set up on the scalp of the subject and the associated waves generated from the various parts are studied.
4. A particular region in the brain which is the most hyperactive will be chosen and more trials will be done on that part alone and the corresponding EEG waves will be analyzed
Equipments:
EEG machine (available at BCI Centre, CSE dept)
Duration:
1 month
Estimated Budget:
NIL
Scope of the study:
It leads to a better understanding of human memory and a probability
To study the patterning of memory in human brain
Theory:
The human brain has 4 lobes. The frontal lobe is for intellectual activity like learning, memorizing, emotion etc. It is not known perfectly how the memorizing process inside a brain takes place. The different lobes play a different role in the fore said process. In this study we try to examine which part of the brain is hyperactive during the learning process. The brain has capability to generate waves which can be detected by EEG. We try to locate a particular area of the brain and waves associated for learning and memorizing by a simple experiment described in the next section. More or less no literature backup is available to support the current study. Hence this paper will have preliminary result to study and localize the memory patterns in the human brain.
Experiment:
1. A suitable candidate is chosen.
2. He is given a paragraph from a unknown source to read and memorize.
3. In this process EEG electrodes are set up on the scalp of the subject and the associated waves generated from the various parts are studied.
4. A particular region in the brain which is the most hyperactive will be chosen and more trials will be done on that part alone and the corresponding EEG waves will be analyzed
Equipments:
EEG machine (available at BCI Centre, CSE dept)
Duration:
1 month
Estimated Budget:
NIL
Scope of the study:
It leads to a better understanding of human memory and a probability of storing data in human brain artificially. The human brain has 4 lobes. The frontal lobe is for intellectual activity like learning, memorizing, emotion etc. It is not known perfectly how the memorizing process inside a brain takes place. The different lobes play a different role in the fore said process. In this study we try to examine which part of the brain is hyperactive during the learning process. The brain has capability to generate waves which can be detected by EEG. We try to locate a particular area of the brain and waves associated for learning and memorizing by a simple experiment described in the next section. More or less no literature backup is available to support the current study. Hence this paper will have preliminary result to study and localize the memory patterns in the human brain.
Experiment:
1. A suitable candidate is chosen.
2. He is given a paragraph from a unknown source to read and memorize.
3. In this process EEG electrodes are set up on the scalp of the subject and the associated waves generated from the various parts are studied.
4. A particular region in the brain which is the most hyperactive will be chosen and more trials will be done on that part alone and the corresponding EEG waves will be analyzed
Equipments:
EEG machine (available at BCI Centre, CSE dept)
Duration:
1 month
Estimated Budget:
NIL
Scope of the study:
It leads to a better understanding of human memory and a probability
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