Junk DNA:
The question of how much of our junk DNA may turn out to be functional is a fascinating topic. I wrote a paper on this topic about 5 years ago based largely on the work of John Mattick. Mattick argues that because most of the genome is actually transcribed, and because it seems to be transcribed in a programmatic way (ie some noncoding areas are transcribed in a pattern dissimilar to adjacent genes) then most of the genome is probably functional. When I wrote the paper, I agreed with this idea but I have a more nuanced position today I think. A few weeks before I finished my report, a paper was published in nature showing that a mouse that had many noncoding regions deleted from its genome was clinically equivalent to other mice. Among the noncoding regions that were deleted from the mouse's genome were areas referred to as "ultra conserved regions." Some UCR's are more conserved in vertebrates than some of the most constant proteins. If these sequences were conserved so pristinely by natural selection, they must have a crucial function. But, this experiment seemed to show that was not the case. But, there is still a mystery here. If these sequences were not crucial for the survival of the mouse, why were they conserved over the course of 100 million years of evolution?
Going back to my notes of Power, Sex, Suicide by Nick Lane, on page 187 he talks about how the extra DNA in eukaryotes may function as raw material for new genes. Bacteria were under selection for trim genomes because fast division was important. It's not that eukaryotes are under selection for bigger genomes so that they can later evolve new genes. Natural selection cannot and does not plan ahead. Therefore, the tendency toward bigger genomes is more likely because mutations that add something, anything to the genome are more likely to be neutral than ones that delete something. Therefore, if eukaryotes are not under selection for small genomes, then they will tend to collect junk over time.
Why our 'junk DNA' may be useful after all:
Pearson, Aria New Scientist; 7/14/2007, Vol. 195 Issue 2612, p42-45, 4p
Finally a balanced and reasonable article on the subject of junk DNA. Pearson points out that we have actually known about functional noncoding DNA since the early 70s. In Mattick's writings, he accuses the scientific establishment of completely ignoring noncoding regions for decades. From what I've been reading, I don't think that this is actually the case. The reason why science has focused on coding regions in because they are better understood and mutations in them are more easily pinpointed.
The article compares junk DNA to bloatware on new computers. Some of it may appear to be doing something and appear to be functional but whether or not it is doing us any good is debatable. This is an interesting analogy and I can't help but think it must be true in many cases.
Many researchers believe that most noncoding RNAs that are transcribed are really just noise that is generated by the transcription of nearby genes. However, Gingeras argues that this can't explain a lot of non coding transcription because many non coding RNAs are transcribed in areas where there are no genes nearby. I wonder if a lot of this is like the bloatware analogy. Perhaps something is happening but that doesn't mean that whatever is happening is necessarily benefiting the organism.
One interesting observation that Mattick makes is that long noncoding RNAs transcribed in the mouse brain are transcribed differently than the genes that they are closest to. This suggests that their transcription is not an accident but must be controlled programmatically.
What this article shows is that the debate is not about whether or not any sequences outside of protein coding sequences are functional. We have known that many are for decades. The debate is about how much will end up being functional. Mattick argues that more than 50% of the genome is functional and perhaps up to 80% or 90% based on the amount of the genome that is transcribed. Other researchers put the estimate at below 5% of the genome and there are plenty in between.
This is a fascinating debate. To me it seems unlikely that Mattick is right. He cannot explain why some species such as the puffer fish can get away with such a trim genome or why some relatively simple organisms such as some species of amoeba have so much junk DNA that their genomes are actually larger than humans.
But, at the same time, even if the most conservative biologists are right, if less than 5% of the genome is functional, that is still a lot of functional non coding DNA that we don't understand yet!
This paper talks about the experiment that deleted ultra conserved regions from the mouse. One explanation that was given was that perhaps the effect of these regions is subtle. If the sequence made the mouse just 1% more likely to survive then it would be preserved. I don't like this explanation. If the effect was really that subtle, then it would be more likely to be able to evolve over time. If these sequences are more preserved then protein coding genes then subtle effects do not explain their preservation.
Another explanation given by Kelly Frazer is that redundancy could be built in and there were other regions that compensated for the ones that were deleted. I don't like this explanation either. If there really is this much redundancy then how could the region be more conserved than protein coding genes? I don't see how natural selection could keep these regions so pristine if there is redundancy in the system.
This is a great mystery to me because I don't agree with any of the explanations put forward. There are many potential angles for my thesis here.
Sean Carroll:
Scientific American May 2008: Regulating Evolution
This article in Scientific American by one of my favorite authors Sean Carroll (Endless Forms Most Beautiful) explores the evolution of "enhancers" which he refers to as "switches." Eukaryotes uniquely promote transcription of their genes through these switches which can appear long before, long after or even with in introns! They are hard to detect experimentally which is why many genetic mutations have been determined to be regulatory in nature even though the exact mutation remains elusive.
The article explores some examples of phenotypes that can be modified by these regulatory sequences without affecting how the gene is expressed in other parts of the body or in other life stages.
One of the main source articles that Carroll references is Wray's paper in nature which I review below:
Gregory Wray: March 2007 Nature Reviews Genetics The evolutionary Significance of cis-regulatory mutations
Wray argues that cis-regulatory and protein coding mutations may be phenotypically distinct. He gives 2 reasons for this.
1. Each allele in a diploid organism is transcribed independently. Therefore, mutations in regulatory regions tend to be co-dominant whereas structural mutations may not be visible to natural selection till genetic drift takes place to the point where there are significant numbers organisms homozygous for the mutation.
2. Cis-regulatory mutations may only affect the organism in particular tissue or life stage whereas structural mutation will affect organism everywhere protein is expressed. There is potential for alternative splicing to cushion this affect but clear examples of this are rare.
One example he discusses is lactose tolerance in adults in northern Europeans. The switch that enabled this was actually located inside a intron in the gene that was affected. This is interesting because Mattick talks a lot about the potential for introns to evolve function. This is a great example of one that did.
Another example comes from comparisons of microarrays of gene expression in the brains of humans and chimps. The levels are expression are different for more than 10% of the genes that are expressed. The author points out that this is actually probably an underestimate. It is unknown where in the genome the regulatory sequences that affected this expression is encoded. Mattick has argued that trans-regulation may be at work, that is regulatory sequences no where near the genes being expressed.
Another example is the increased expression of prodynorphin in humans relative to other primates. This gene is involved in emotional status and perception of pain. A mutation in the regulatory sequence of this gene is responsible for the increased expression in humans.
I have a lot of material to digest here. There are a lot of angles I can take this. Mattick may be wrong that most of the genome is functional, but from what I am reading that may not matter. Even if only a small percentage is functional that doesn't change the fact that noncoding sequences may be the main drivers of eukaryotic evolution.
Monday, March 8, 2010
Monday, March 1, 2010
Junk DNA and the foundation of eukaryotic complexity
I've been considering some new ideas for my capstone thesis. In 2004 for my science writing class, I wrote a paper about the possible function of Junk DNA. You can download and read my paper here. I was reluctant to post it because when I reread it now I don't necessarily agree with all of the conclusions that I came to. Now, I think that the idea that most junk DNA is regulatory is probably just wrong. I argued that biological complexity scales better with genome size than with gene count and that perhaps some junk DNA has a regulatory function. I explored the potential roles that micro RNAs, RNA interference and introns might play in the specification of complexity in higher eukaryotes. My main reference was the work of John Mattick who argued that the genome may contain regulatory networks he called Endogenous Controlled Multitasking. I just did a search on him on nature.com and he has done a lot more work since I last looked at him mostly in the area of micro RNAs. This week, I am going to spend some time catching up on this stuff. I think it has a great potential to turn into my thesis. Even though my original idea might have been wrong, this is still a hot area. Perhaps a small percentage of junk DNA is functional. It doesn't all have to be functional for this to be an interesting area for study!
Sunday, February 21, 2010
Further reading
I have been reading some journal articles referenced in the back of Power, Sex, Suicide under further reading to get some more background on Lane's mitochondrial aging ideas. Here's a short summary of what I have so far:
"Living Fast, Dying When?" Article from Waltham International Symposium
This article investigates evidence that correlates metabolic rate with aging. Argues that rise in resting metabolic rate extends life (decoupling in Lane’s book) while rise in nonresting rate decreases lifespan.
"Uncoupled and Surviving" From Journal Aging Cell 2004
This article studies mice with varying levels of metabolism and argues that those with more uncoupling live longer. However, from reading the article it appears that trying to infer rate of uncoupling would be technically very difficult. I will have to do some more research to find out if it is possible.
"Aging Studies On Bats: A Revew" From Biogerontology 2004
This article discusses bats as a model for aging studies. I haven't finished this one yet but it has some good potential. Bats have longer life stages similar to primates and they share flight with birds. It is interesting that they also put off aging.
"Living Fast, Dying When?" Article from Waltham International Symposium
This article investigates evidence that correlates metabolic rate with aging. Argues that rise in resting metabolic rate extends life (decoupling in Lane’s book) while rise in nonresting rate decreases lifespan.
"Uncoupled and Surviving" From Journal Aging Cell 2004
This article studies mice with varying levels of metabolism and argues that those with more uncoupling live longer. However, from reading the article it appears that trying to infer rate of uncoupling would be technically very difficult. I will have to do some more research to find out if it is possible.
"Aging Studies On Bats: A Revew" From Biogerontology 2004
This article discusses bats as a model for aging studies. I haven't finished this one yet but it has some good potential. Bats have longer life stages similar to primates and they share flight with birds. It is interesting that they also put off aging.
Tuesday, February 9, 2010
Lane himself weighs in!
After discussing my human hairlessness idea with my professor last night, I sent the following email to Dr Lane last night asking what he thought about it and whether or not it made sense:
Dr Lane,
I am an undergrad at Utah Valley University studying bioinformatics and a big fan of your books! Last year, one of my professors turned me on to Life Ascending I couldn't put it down. I am trying to nail down a topic for an undergraduate thesis and I have an idea from Power, Sex, Suicide and was was curious whether or not you or anyone else has ever thought about this and if it makes sense in the first place.
I have been looking into the issue of human hairlessness. In this months issue of Scientific American Jablanski argues that a combination of hairlessness and specialized sweat glands evolved to prevent overheating while chasing down prey on open savanna.
At the end of Power, Sex, Suicide, you talk about the fact that humans already live several times longer than we should for our size and suggest that perhaps similar to birds, but not to the same extent, we may have already increased our lifespan by increasing our mitochondrial capacity and increasing our sensitivity to free radical signalling.
You suggest that this selection possibly occurred because extended lifespan enabled elders to pass on important information to their descendants.
If this is true, then wouldn't it follow that humans are generating more heat? I know there are debates in the literature about whether or not the heat of the open savanna would be enough to explain the evolution of hairlessness in humans. What I am wondering, is if your idea that humans may have increased mitochondrial capacity may have tipped the scales in favor of hairlessness because of the combination of extra heat generated by increased mitochondrial capacity and the heat of the open savanna.
So, I am wondering if linking these 2 things makes any sense at all. As you mention in your book birds do have a slightly higher body temperature because of their higher capacity. Does it make sense to assume that humans generate slightly more heat than other mammals of similar size and as such would have more of a reason to go hairless?
Dr Lane's response:
That's a very interesting idea. The short answer is it certainly makes sense as an idea, but I've never heard of any data that would support it. But all that means is that I think the body temperature of a gorilla is around 37C, as is our own. And as you say, we would lose more heat than a gorilla simply because we are hairless, and so it follows that they would be the same.
Excellent idea! How to test it? I suppose you'd need accurate information on mitochondrial density in different tissues; ideally the level of uncoupling (possibly similar if the difference in heat production comes down to mito density, where all mitos are leaking at the same rate); rate of heat transfer across the skin with or without hair at say 40 degrees; and body temperature (again, I assume it would be similar but the rate of heat production and heat transfer would be different). I suppose other factors might be prevailing wind, height, etc - climatic factors that might alter heat transfer, and which you might take into consideration in terms of the geography of where and when modern hairless humans evolved. Also, any info on lifespan would be useful is australopithecines vs homo sapiens, etc.
I doubt that you could track down much of this information in the time available for your project, but you can probably discuss it all in an open-ended way, and take a stab at realistic values where possible.
Good luck! Best wishes
Nick
Dr Lane,
I am an undergrad at Utah Valley University studying bioinformatics and a big fan of your books! Last year, one of my professors turned me on to Life Ascending I couldn't put it down. I am trying to nail down a topic for an undergraduate thesis and I have an idea from Power, Sex, Suicide and was was curious whether or not you or anyone else has ever thought about this and if it makes sense in the first place.
I have been looking into the issue of human hairlessness. In this months issue of Scientific American Jablanski argues that a combination of hairlessness and specialized sweat glands evolved to prevent overheating while chasing down prey on open savanna.
At the end of Power, Sex, Suicide, you talk about the fact that humans already live several times longer than we should for our size and suggest that perhaps similar to birds, but not to the same extent, we may have already increased our lifespan by increasing our mitochondrial capacity and increasing our sensitivity to free radical signalling.
You suggest that this selection possibly occurred because extended lifespan enabled elders to pass on important information to their descendants.
If this is true, then wouldn't it follow that humans are generating more heat? I know there are debates in the literature about whether or not the heat of the open savanna would be enough to explain the evolution of hairlessness in humans. What I am wondering, is if your idea that humans may have increased mitochondrial capacity may have tipped the scales in favor of hairlessness because of the combination of extra heat generated by increased mitochondrial capacity and the heat of the open savanna.
So, I am wondering if linking these 2 things makes any sense at all. As you mention in your book birds do have a slightly higher body temperature because of their higher capacity. Does it make sense to assume that humans generate slightly more heat than other mammals of similar size and as such would have more of a reason to go hairless?
Dr Lane's response:
That's a very interesting idea. The short answer is it certainly makes sense as an idea, but I've never heard of any data that would support it. But all that means is that I think the body temperature of a gorilla is around 37C, as is our own. And as you say, we would lose more heat than a gorilla simply because we are hairless, and so it follows that they would be the same.
Excellent idea! How to test it? I suppose you'd need accurate information on mitochondrial density in different tissues; ideally the level of uncoupling (possibly similar if the difference in heat production comes down to mito density, where all mitos are leaking at the same rate); rate of heat transfer across the skin with or without hair at say 40 degrees; and body temperature (again, I assume it would be similar but the rate of heat production and heat transfer would be different). I suppose other factors might be prevailing wind, height, etc - climatic factors that might alter heat transfer, and which you might take into consideration in terms of the geography of where and when modern hairless humans evolved. Also, any info on lifespan would be useful is australopithecines vs homo sapiens, etc.
I doubt that you could track down much of this information in the time available for your project, but you can probably discuss it all in an open-ended way, and take a stab at realistic values where possible.
Good luck! Best wishes
Nick
Sunday, February 7, 2010
The naked truth
Why are humans hairless? An article in the journal of Zoology: Evolution of nakedness in Homo sapiens by Rantala puts forth quote a few ideas and their associated weaknesses. You can access the whole article in full here. Here are some of the ideas in the article:
The cooling device hypothesis:
We lost our hair to help us cool down in dry savannas. However Rantala argues that in the day time exposed skin actually receives more solar energy. Also increases perspiration which may cause dehydration which is very bad in savanna. He points out that savanna monkeys actually have increased hair coverage which is what we should expect.
The hunting hypothesis (otherwise known as running hypothesis)
This one says that carnivorous hominids would need to go hairless because they have to chase down their prey. Other primates (presumably these savanna monkeys) are vegetarians and don’t have to move as fast. But again, this hypothesis once again assumes that naked skin is really a good way to cool down (there must be evidence that it is if so many accept this.) Also, if this were true, and males were the hunters, why are females even more hairless?
Allometry hypothesis:
Not all organs increase in the same proportions as animals get bigger. Since humans evolved from smaller apes, the hair got sparser and as it did, sweat became the new coolant and fur became useless. The problem with this one is that gorillas hairs are further apart but they have a thick luxurious coat.
The vestiary hypothesis:
Hairlessness evolved alongside bigger brains and culture which allowed us to use clothing to regulate heat. Rantala doesn't like this one either because he believes that it's also based on faulty cooling factor.
Neoteny hypothesis:
Humans are juvenilized apes and hairlessness was just part of that package. Richard Dawkins points out in his new book "The Greatest Show On Earth" that adult humans share many features with juvenile apes. Perhaps hairlessness came with that package? This is unlikely because not all juvenile ape features are beneficial and natural selection has only retained the beneficial ones.
Adaptation against ectoparasites hypothesis:
One problem with a parasite hypothesis is that all apes have problems with parasites. What makes humans so special? Well the answer is that As humans began to establish base camps, fleas and other parasites became a bigger problem. Diseases caused by these parasites would have had strong selective pressure toward naked skin. Alan Rogers (University of Utah) did some research on the evolution of skin color (MC1R gene) and dates darker skin to about 1.2 million years ago. This is consistent with the time we started to occupy base camps.
The parasite idea is the one that the author likes best. It makes sense and I am sure that there is at least some truth to it. However, I believe that Rantala is mistaken about naked skin being a bad way to cool the body. Dennis Bramble at the University of Utah has been researching on this topic for a while. Here is a paper on The Evolution of Marathon Running. Bramble's research shows that on a hot day, a human could out compete a horse in a marathon. I think the problem with Rantala is that he does not account for our specialized sweat glands which are much different than other primates.
I think that there is probably truth to the parasite idea and the running idea. However, I don't think that these things themselves are the whole story. In my previous "tying it all together" post I have talked about Lane's idea that perhaps humans have increased mitochondrial capacity which was selected for to increase lifespan because of the knowledge advantages that elders provide. Raising internal heat generation lowers free radical formation at rest which in turn increases lifespan. If this is true, then this could make overheating a bigger problem. So far, I can't find any literature linking increased mitochondrial capacity to human hairlessness but I think it is certainly possible. This is an exciting possible angle for my thesis!
The cooling device hypothesis:
We lost our hair to help us cool down in dry savannas. However Rantala argues that in the day time exposed skin actually receives more solar energy. Also increases perspiration which may cause dehydration which is very bad in savanna. He points out that savanna monkeys actually have increased hair coverage which is what we should expect.
The hunting hypothesis (otherwise known as running hypothesis)
This one says that carnivorous hominids would need to go hairless because they have to chase down their prey. Other primates (presumably these savanna monkeys) are vegetarians and don’t have to move as fast. But again, this hypothesis once again assumes that naked skin is really a good way to cool down (there must be evidence that it is if so many accept this.) Also, if this were true, and males were the hunters, why are females even more hairless?
Allometry hypothesis:
Not all organs increase in the same proportions as animals get bigger. Since humans evolved from smaller apes, the hair got sparser and as it did, sweat became the new coolant and fur became useless. The problem with this one is that gorillas hairs are further apart but they have a thick luxurious coat.
The vestiary hypothesis:
Hairlessness evolved alongside bigger brains and culture which allowed us to use clothing to regulate heat. Rantala doesn't like this one either because he believes that it's also based on faulty cooling factor.
Neoteny hypothesis:
Humans are juvenilized apes and hairlessness was just part of that package. Richard Dawkins points out in his new book "The Greatest Show On Earth" that adult humans share many features with juvenile apes. Perhaps hairlessness came with that package? This is unlikely because not all juvenile ape features are beneficial and natural selection has only retained the beneficial ones.
Adaptation against ectoparasites hypothesis:
One problem with a parasite hypothesis is that all apes have problems with parasites. What makes humans so special? Well the answer is that As humans began to establish base camps, fleas and other parasites became a bigger problem. Diseases caused by these parasites would have had strong selective pressure toward naked skin. Alan Rogers (University of Utah) did some research on the evolution of skin color (MC1R gene) and dates darker skin to about 1.2 million years ago. This is consistent with the time we started to occupy base camps.
The parasite idea is the one that the author likes best. It makes sense and I am sure that there is at least some truth to it. However, I believe that Rantala is mistaken about naked skin being a bad way to cool the body. Dennis Bramble at the University of Utah has been researching on this topic for a while. Here is a paper on The Evolution of Marathon Running. Bramble's research shows that on a hot day, a human could out compete a horse in a marathon. I think the problem with Rantala is that he does not account for our specialized sweat glands which are much different than other primates.
I think that there is probably truth to the parasite idea and the running idea. However, I don't think that these things themselves are the whole story. In my previous "tying it all together" post I have talked about Lane's idea that perhaps humans have increased mitochondrial capacity which was selected for to increase lifespan because of the knowledge advantages that elders provide. Raising internal heat generation lowers free radical formation at rest which in turn increases lifespan. If this is true, then this could make overheating a bigger problem. So far, I can't find any literature linking increased mitochondrial capacity to human hairlessness but I think it is certainly possible. This is an exciting possible angle for my thesis!
Friday, February 5, 2010
The blank slate
I bought Steven Pinker's book The Blank Slate: The Modern Denial of Human Nature last semester when researching a paper about cultural evolution. I only had time to flip through it but didn't have time to read it. But, it just barely came out in audio so now I am listening to it. It's an important topic because we could never understand human evolution if we don't acknowledge human nature. Pinker's main assertion is that political radicals in academia push this idea about the human brain being a blank slate devoid of innate structure that is molded only by experience and social interaction and that these ideas have bled over into the hard sciences. This idea is really a secular religion based on the philosophy of Marx since there is no scientific reason to assume that we aren't born with innate faculties.
One problem so far is that the name seems to be somewhat of a straw man. I don't think that everyone he criticizes really believes that the brain has no innate structure at all. He seems very offended about the biological determinist straw man that the other side uses to paint him and I can't help but think that maybe he is doing the same thing at least to some extent. However, I know that the kind of people he talks about exist. I have had some really lefty professors that didn't seem to understand how evolution works always deferring to Gould on the topic and really fit into this blank slate mentality Pinker is talking about.
Also, Pinker seems to want it both ways which makes things confusing. He repeatedly defends the writings of Herrnstein (The Bell Curve) then elsewhere says that race need not be invoked to explain differences among groups.
One problem so far is that the name seems to be somewhat of a straw man. I don't think that everyone he criticizes really believes that the brain has no innate structure at all. He seems very offended about the biological determinist straw man that the other side uses to paint him and I can't help but think that maybe he is doing the same thing at least to some extent. However, I know that the kind of people he talks about exist. I have had some really lefty professors that didn't seem to understand how evolution works always deferring to Gould on the topic and really fit into this blank slate mentality Pinker is talking about.
Also, Pinker seems to want it both ways which makes things confusing. He repeatedly defends the writings of Herrnstein (The Bell Curve) then elsewhere says that race need not be invoked to explain differences among groups.
Monday, February 1, 2010
Tying it all together
So, do our mitochondria really kill us in the end? According to the mitochondrial theory of aging, we should expect to find cells full of worn out mitochondria as we grow old. Lane says that this is not what we find. Worse, most of the diseases associated with aging have been linked to nuclear genes.
However, Lane goes on to explain that as mitochondria become damaged through mutation they are displaced by healthy ones that begin to divide. When a cell is completely riddled with damaged mitochondria, it commits apoptosis. This is why we don't see a build up of mutations, but instead see that organs begin to wither away. The surviving healthy tissue is now under increased stress. This explains why aging diseases are due to mutations in the nuclear genes and is a good clue to why trying to cure them all one by one is futile. The diseases of aging simply add stress to tissues that are already under duress due to loss of cells that committed apoptosis because of worn out mitochondria. If the mitochondria were healthy and the tissue were not withering away, we would not succumb to the diseases of aging. The whole aging process could be delayed as it is in birds. So what is different about birds? Why do they live so long? Lane goes on to explain that birds have far less free radical leakage in their mitochondria. This problem sounds simple enough. Doesn't this mean that more antioxidants should solve the problem? Not so fast, says Lane. Free radicals are actually an important signal that helps regulate energy production. Therefore, if we wish to extend lifespan by reducing free radical leakage, then the chemical receptors that detect free radicals must be enhanced to be more sensitive so that these signals are not blotted out. This is why rats have such a short lifespan. having a more refined detection system is a big evolutionary feat and there has to be a payoff a lot bigger than just extended life. Birds do have a special need: powered flight. Lane also points out that while humans don't live nearly as long as birds, we are much better off than other similarly sized mammals. So that means humans must have recently been under strong selection for longer lifespans and probably already have more sensitive
free radical detection equipment than other mammals. Lane believes that we might find we could significantly increase lifespan by tweaking just a few genes.
So what special selection pressure have humans been under for longer lifespan? It could have been a feedback loop of caring for their elderly and selection for longer lifespan. Therefore, there would be selection for behavior where humans tend to care for those who cannot care for themselves. In my last post, I linked this kind of caring with a tendency to have compassion and care for all disabled including our children. See, I told you I'd tie it all together!
However, Lane goes on to explain that as mitochondria become damaged through mutation they are displaced by healthy ones that begin to divide. When a cell is completely riddled with damaged mitochondria, it commits apoptosis. This is why we don't see a build up of mutations, but instead see that organs begin to wither away. The surviving healthy tissue is now under increased stress. This explains why aging diseases are due to mutations in the nuclear genes and is a good clue to why trying to cure them all one by one is futile. The diseases of aging simply add stress to tissues that are already under duress due to loss of cells that committed apoptosis because of worn out mitochondria. If the mitochondria were healthy and the tissue were not withering away, we would not succumb to the diseases of aging. The whole aging process could be delayed as it is in birds. So what is different about birds? Why do they live so long? Lane goes on to explain that birds have far less free radical leakage in their mitochondria. This problem sounds simple enough. Doesn't this mean that more antioxidants should solve the problem? Not so fast, says Lane. Free radicals are actually an important signal that helps regulate energy production. Therefore, if we wish to extend lifespan by reducing free radical leakage, then the chemical receptors that detect free radicals must be enhanced to be more sensitive so that these signals are not blotted out. This is why rats have such a short lifespan. having a more refined detection system is a big evolutionary feat and there has to be a payoff a lot bigger than just extended life. Birds do have a special need: powered flight. Lane also points out that while humans don't live nearly as long as birds, we are much better off than other similarly sized mammals. So that means humans must have recently been under strong selection for longer lifespans and probably already have more sensitive
free radical detection equipment than other mammals. Lane believes that we might find we could significantly increase lifespan by tweaking just a few genes.
So what special selection pressure have humans been under for longer lifespan? It could have been a feedback loop of caring for their elderly and selection for longer lifespan. Therefore, there would be selection for behavior where humans tend to care for those who cannot care for themselves. In my last post, I linked this kind of caring with a tendency to have compassion and care for all disabled including our children. See, I told you I'd tie it all together!
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