for my Evolution capstone course, we are each supposed to bring in an argument against evolution which according to the professor will fall into 1 of 3 categories. I know I've heard this before but I don't remember what they were. Anyway, I'm sure most of the examples that students will bring in will be from intelligent design advocates associated with the religious right. However, according to Kenneth Miller, in his book Only a theory, many of the creationist arguments that come from the religious right were actually borrowed from the extreme academic left. Case in point, a recent book that Nature called a "misguided attack on evolution", What Darwin Got Wrong by philosopher Jerry Fodor is a great example. His central argument is that natural selection cannot tell the difference between adaptive traits and freeloader traits. I have addressed this topic at length in previous posts and I believe it is a pretty inane claim coming from such a supposedly sophisticated philosopher. I don't believe that there is a meaningful distinction between a selfish freeloading trait and a truly adaptive trait (see my last few posts on this topic.)
Another claim he makes is that evolution is a historical process and as such isn't truly testable. I like the way that Nick Lane addresses this claim in his book Life Ascending in his chapter on the evolution of the vertebrate eye. He points out that when investigating the evolution of a particular phenotype, we actually can make specific predictions. It doesn't matter that the process actually occurred long ago. The fact is, we can make predictions about how some structure evolved and we can confirm or falsify these claims as the data comes in from genome sequences and other sources. For example, we can make the claim that the vertebrate eye evolved by the process of natural selection. The common ancestor of invertebrate chordates and vertebrates did have a retina. In fact, the sea squirt today has a retina but no lens. So, to confirm this claim we would need to show that the specialized lens proteins that exist in the vertebrate eye were already present in this common ancestor. What is important to note here is that these kinds of claims are definitely falsifiable. If these apparently specialized proteins just appeared out of thin air, that would be a huge blow to natural selection. Potentially, if such a pattern emerged, then evolution by natural selection could be falsified. But, according to Lane, this is not what was found. He explains that vertebrate eye crystallin proteins were sequenced in the 80s and all of the proteins used to construct the vertebrate eye can be found in other parts of the body fulfilling other completely unrelated tasks. In fact, in the sea squirt which does not have a lens over its retina, some of these crystallin proteins are performing other functions nearby in the brain. This example is not isolated of course and there are many different ways that predictions can be made about the path that natural selection has taken which can then be tested as data becomes available. Fodor's criticism is indeed misguided.
Sunday, May 9, 2010
Thursday, April 29, 2010
Bioinformatic analysis of Ephemeroptera
This semester I have been creating a workflow using Taverna to help Dr. Ogden at UVU with his analysis of mayflies and dragonflies.
Taverna is a platform used to create scientific workflows. There is a drag and drop interface where existing services can be drug to the workflow and integrated with your experiment. Taverna integrates with MyExperiment which makes it easy to publish and share your workflows. Dr Ogden has a particular problem he is trying to solve with his research that has not been addressed yet using this platform so many custom components have to be developed using Java in order to complete this project. This semester, I got something working but there is still a lot of work to do.
My workflow needs to be smart enough to automatically create a merged dataset for any order specified but also flexible enough that the user can customize the way that the data set is created and analyzed. Currently, a lot of time is spent manually creating these datasets and this project will not only speed up this process but make the research more traceable and consistent.
Dr Ogden was impressed by my demo and believes that this project may be publishable. Currently, there are not workflow components out there this fill this need. If I make this workflow and the components flexible enough, then other researchers may be able to easily integrate them into their own research projects and this could potentially be a big contribution to the bioinformatics community!
Taverna is a platform used to create scientific workflows. There is a drag and drop interface where existing services can be drug to the workflow and integrated with your experiment. Taverna integrates with MyExperiment which makes it easy to publish and share your workflows. Dr Ogden has a particular problem he is trying to solve with his research that has not been addressed yet using this platform so many custom components have to be developed using Java in order to complete this project. This semester, I got something working but there is still a lot of work to do.
My workflow uses queries genbank and gets all of the sequences for the Ephemeroptera order. It then extracts the taxa and the element name from each one. There are a lot of duplicates so it then sorts these by date and gets the most recent, also if one sequence is marked as complete and another as partial it will use the complete one. For each element, if there are enough taxa for it, it will create a dataset for that element. Wingless for example only has 3 taxa so that one is skipped.
Then it does a multiple alignment for each dataset. After that, it creates a merged dataset, for all of the taxa that appear in enough of the datasets (if a given taxa doesn't appear in enough of the individual datasets it is left out.)
The next step is to do a phylogenetic analysis on the final merged dataset. I am still experimenting with how to do this. Taverna likes to do everything with webservices but this dataset is large so that might not be practical. So, it would probably be best to fire off a mr bayes or paup block on the local machine. Anyway, that part is relatively easy anyway.
Over the summer I will be experimenting with creating a slick web interface which I will design using Open Lazlo technology which is a rich web interface programming language that I have been learning on the side.
My workflow needs to be smart enough to automatically create a merged dataset for any order specified but also flexible enough that the user can customize the way that the data set is created and analyzed. Currently, a lot of time is spent manually creating these datasets and this project will not only speed up this process but make the research more traceable and consistent.
Dr Ogden was impressed by my demo and believes that this project may be publishable. Currently, there are not workflow components out there this fill this need. If I make this workflow and the components flexible enough, then other researchers may be able to easily integrate them into their own research projects and this could potentially be a big contribution to the bioinformatics community!
Monday, April 26, 2010
Alu elements and uniquely human traits
Just finished a paper about alu proliferation in primates and the connection to higher cognition in humans. I hope you like it! Download it here
Monday, April 5, 2010
Did population bottlenecks 1mya and before the great leap forward accelerate human evolution?
Here is a possible question for my paper:
Did population bottlenecks 1mya and before the great leap forward accelerate human evolution?
Han and Xing argue in their 2005 paper, Under the genomic radar, that the capacity for alu proliferation can lurk in the primate genome for millions of years. This is because a low activity variant known as a stealth driver may occasionally spawn a high activity daughter sequence. These daughter sequences and it's spawn are likely to be purged by natural selection but the parent stealth driver would be untouched. It would not be active enough itself for natural selection to even be able to see it. In this sense Alu sequences have evolved to subvert natural selection. If Hedges is correct, then even this highly active daughter sequence might be able to subvert natural selection if there is a population bottleneck. In such a bottleneck, these highly active daughter sequences would be permitted to wreak their havoc while any disastrous insertions would have to be selected out one by one. Therefore, population bottlenecks promote alu proliferation. (See my more detailed summary of these 2 articles in my previous post: Did we evolve to evolve?)
In their 2009 article "Mobile elements reveal small population size in the ancient ancestors of Homo sapiens" Huff, Rogers, et al up at the University of Utah compared the complete genomes of 2 individuals. They say that back in the 80s it was predicted that regions of the genome with a rare insertion event (such as an alu insertion) are twice as old as regions without such an event. This is true because a region with such an event has 2 sub-regions one before and one after. They observed that regions with an insertion event had twice the nucleotide diversity which confirms this idea. They determined that the average time since the most recent common ancestor for regions with an insertion event was just under a million years (half this for other regions.) By studying these regions they were able to determine which high confidence that the effective population size a million years ago was less than 26,000 and probably closer to 18,500. This surprisingly low number may be explained by a series of population bottlenecks or different competing populations of homo replacing one another.
Now, this paper used alu sequence data as a marker to determine that there was a population bottleneck a million years ago. It doesn't say anything about the possibility that this bottleneck facilitated increased alu proliferation which is what I would expect from reading Xing and Hedges. Whether or not I can connect these 2 things is something that I will have to determine.
In another 2009 paper from the U "Mobile elements create structural variation" Xing, Huff, et al show how alu proliferation can contribute to structural variation in the human genome. They compared sequences in the HuRef sequencing project to those from the human genome project. They focused on insertions and deletions that were particular to the HuRef genome so that they could identify structural variations that are polymorphic in humans. They found that as many as a third of these polymorphic alu insertions occurred within genic regions. However,all but 3 were not within exons. But as I discussed in previous posts, alu sequences within introns have been shown in some cases to regulate the expression of the parent gene so I believe these variations could potentially be significant. I have a lot of literature supporting this stuff. Also, as Wray (see previous post) argues phenotypic variation arising from regulatory changes may be more directly shapable by natural selection because they tend to be co-dominant.
My next step is to find the connection between the literature about bottlenecks facilitating proliferation and this stuff about alu sequences generating structural variation in the genome. Is there something I can test here using sequence data available on genbank? The accession numbers for the alus studied in the structural varation paper are on there, what can I do with them?
After I have connected those things, then I want to show that selection for higher cognition molded the human brain from this novel variation.
To sum up what I have to work with so far:
Rogers et al: Analyzing alu sequence insertions can tell us about past population bottlenecks
Han and Xing: The stealth driver model predicts that these bottlenecks promote alu proliferation
Xing Huff: Alu proliferation creates structural variation (This is the part that I think I will be able to do some sequence analysis. All of the alus studied in the paper are in genbank)
I have lots of material explaining how natural selection can take advantage of this varation (exonization, alternative splicing, A-I editing, etc) to build the human brain.
In connecting all of these things, I want to answer the question at the top of this post. Did past bottlenecks, accelerate alu proliferation and more importantly, was this extra variation needed to produce the human brain? Or in other words is it selection pressure which determines the outcome or is natural selection constrained by available materials?
Did population bottlenecks 1mya and before the great leap forward accelerate human evolution?
Han and Xing argue in their 2005 paper, Under the genomic radar, that the capacity for alu proliferation can lurk in the primate genome for millions of years. This is because a low activity variant known as a stealth driver may occasionally spawn a high activity daughter sequence. These daughter sequences and it's spawn are likely to be purged by natural selection but the parent stealth driver would be untouched. It would not be active enough itself for natural selection to even be able to see it. In this sense Alu sequences have evolved to subvert natural selection. If Hedges is correct, then even this highly active daughter sequence might be able to subvert natural selection if there is a population bottleneck. In such a bottleneck, these highly active daughter sequences would be permitted to wreak their havoc while any disastrous insertions would have to be selected out one by one. Therefore, population bottlenecks promote alu proliferation. (See my more detailed summary of these 2 articles in my previous post: Did we evolve to evolve?)
In their 2009 article "Mobile elements reveal small population size in the ancient ancestors of Homo sapiens" Huff, Rogers, et al up at the University of Utah compared the complete genomes of 2 individuals. They say that back in the 80s it was predicted that regions of the genome with a rare insertion event (such as an alu insertion) are twice as old as regions without such an event. This is true because a region with such an event has 2 sub-regions one before and one after. They observed that regions with an insertion event had twice the nucleotide diversity which confirms this idea. They determined that the average time since the most recent common ancestor for regions with an insertion event was just under a million years (half this for other regions.) By studying these regions they were able to determine which high confidence that the effective population size a million years ago was less than 26,000 and probably closer to 18,500. This surprisingly low number may be explained by a series of population bottlenecks or different competing populations of homo replacing one another.
Now, this paper used alu sequence data as a marker to determine that there was a population bottleneck a million years ago. It doesn't say anything about the possibility that this bottleneck facilitated increased alu proliferation which is what I would expect from reading Xing and Hedges. Whether or not I can connect these 2 things is something that I will have to determine.
In another 2009 paper from the U "Mobile elements create structural variation" Xing, Huff, et al show how alu proliferation can contribute to structural variation in the human genome. They compared sequences in the HuRef sequencing project to those from the human genome project. They focused on insertions and deletions that were particular to the HuRef genome so that they could identify structural variations that are polymorphic in humans. They found that as many as a third of these polymorphic alu insertions occurred within genic regions. However,all but 3 were not within exons. But as I discussed in previous posts, alu sequences within introns have been shown in some cases to regulate the expression of the parent gene so I believe these variations could potentially be significant. I have a lot of literature supporting this stuff. Also, as Wray (see previous post) argues phenotypic variation arising from regulatory changes may be more directly shapable by natural selection because they tend to be co-dominant.
My next step is to find the connection between the literature about bottlenecks facilitating proliferation and this stuff about alu sequences generating structural variation in the genome. Is there something I can test here using sequence data available on genbank? The accession numbers for the alus studied in the structural varation paper are on there, what can I do with them?
After I have connected those things, then I want to show that selection for higher cognition molded the human brain from this novel variation.
To sum up what I have to work with so far:
Rogers et al: Analyzing alu sequence insertions can tell us about past population bottlenecks
Han and Xing: The stealth driver model predicts that these bottlenecks promote alu proliferation
Xing Huff: Alu proliferation creates structural variation (This is the part that I think I will be able to do some sequence analysis. All of the alus studied in the paper are in genbank)
I have lots of material explaining how natural selection can take advantage of this varation (exonization, alternative splicing, A-I editing, etc) to build the human brain.
In connecting all of these things, I want to answer the question at the top of this post. Did past bottlenecks, accelerate alu proliferation and more importantly, was this extra variation needed to produce the human brain? Or in other words is it selection pressure which determines the outcome or is natural selection constrained by available materials?
Monday, March 29, 2010
the role of alu sequences in uniquely human traits
One way that alu sequences are recruited into the functional genome is through a process called exonization.
Lei and Day explain that alu elements actually contain enhancer sequences that facilitate this process.
Ha¨sler and Katharina Strub explain that many alus are found within coding regions of genes. They get there through exonization. This can happen when an alu is inserted in the middle of an intronic region resulting in a new exon. There are several possibilities for alternative splicing in this scenario. Perhaps only the alu sequence itself is included in the new exon or the portion of the intron upstream or downstream could potentially be included. Not all potential splice sites are employed at the same frequency. This is evidence of selection shaping how these genes are alternatively spliced. Another interesting thing is that in every case, some kind of alternative splicing occurs in every gene that contains an exonized alu. The addition of a new exon into a gene would probably involve a frameshift and would be presumably deleterious. So, perhaps unless the original gene is preserved through alternative splicing any new configuration is eliminated through selection.
The exonization process depends on multiple subsequent mutations. These have been mapped out in some cases by Singer and Shmitz in their paper: From Junk to Gene. I wasn't able to look at the whole article yet, because I am waiting for the interlibrary loan but they actually map out the exact sequence of steps involved in the exonization of some particular alu sequences which is pretty amazing.
Since exonization events depend on multiple successive mutations and almost all of the time there will be no benefit for the organism there would need to be a large pool of proliferating alus to draw from in order to explore all of the possibilities. The human genome contains over a million such sequences.
Another area I have been reading about is in the role of alus in RNA editing. Eisenberg explains that in addition to sometimes changing the products of mRNA transcripts, RNA editing may subtly effect the stability of the RNA molecule which in the end would effect expression.
Mattick links alu sequences to the function of memory formation in the human brain. He points out that the ADAR2 protein which is involved in RNA editing binds to alu sequences. ADAR2 is linked to cell signaling pathways involved in memory formation. Mattick believes that this may be a way that an organisms environment and an individual's experiences can shape the way memories are formed.
Gommans and Maas describe RNA editing in terms of evolvability. They argue that selection may favor systems with high levels of diversity and that the drive toward complexity may arise from the need to keep selfish elements under control. They argue that the more complex an organism is, the more resilient it is against the effects of RNA editing. This inevitably leads to tolerance and proliferation of alus that induce RNA editing. This new editing increases the complexity of the organism even more which results in a feedback loop of ascending complexity.
The debate about how much of the noncoding genome is functional is fundamentally misguided. In the case of transposable elements in general and alus in particular, all are in some sense evolutionarily successful or they would not be there at all. But are they functional? I suppose it depends on your perspective. I am reminded of Lane's musings on the troubled birth of the individual. While they generally share the same interests, even the cells in our own body cannot cooperate without mechanisms in place to force them into compliance. All of the genes and other elements in the genome also have a strong incentive to cooperate because if the organism dies then none of them are passed on. But, all elements in the genome must balance these common interests with their own individual interests and unlike rebellious cancerous cells which will never break free, selfish genetic elements are free to evolve and explore ways to pass themselves on. To survive, all elements in the genome must find ways to pass themselves on. So, if a transposable element is recruited by natural selection to perform some function, this element has not lost some kind of battle. From it's perspective, this is the best thing that can happen as being recruited to a task grants the element job security. The same thing happens when a protein coding gene is duplicated. The newly spawned gene must contribute something useful or risk being thrown out by natural selection. Whether you think of the individual in terms of a colony of cells or a group of genes, nothing noteworthy, beautiful or complex can arise without some kind of conflict among the constituent parts. Natural selection does not just magically push life toward complexity. Conflict in the genome isn't about "parasitic" sequences "invading" the genome. Rather, it is about millions of elements cooperating, if reluctantly, to form a cohesive whole. Without conflict, natural selection would have nothing to work with at all.
Lei and Day explain that alu elements actually contain enhancer sequences that facilitate this process.
Ha¨sler and Katharina Strub explain that many alus are found within coding regions of genes. They get there through exonization. This can happen when an alu is inserted in the middle of an intronic region resulting in a new exon. There are several possibilities for alternative splicing in this scenario. Perhaps only the alu sequence itself is included in the new exon or the portion of the intron upstream or downstream could potentially be included. Not all potential splice sites are employed at the same frequency. This is evidence of selection shaping how these genes are alternatively spliced. Another interesting thing is that in every case, some kind of alternative splicing occurs in every gene that contains an exonized alu. The addition of a new exon into a gene would probably involve a frameshift and would be presumably deleterious. So, perhaps unless the original gene is preserved through alternative splicing any new configuration is eliminated through selection.
The exonization process depends on multiple subsequent mutations. These have been mapped out in some cases by Singer and Shmitz in their paper: From Junk to Gene. I wasn't able to look at the whole article yet, because I am waiting for the interlibrary loan but they actually map out the exact sequence of steps involved in the exonization of some particular alu sequences which is pretty amazing.
Since exonization events depend on multiple successive mutations and almost all of the time there will be no benefit for the organism there would need to be a large pool of proliferating alus to draw from in order to explore all of the possibilities. The human genome contains over a million such sequences.
Another area I have been reading about is in the role of alus in RNA editing. Eisenberg explains that in addition to sometimes changing the products of mRNA transcripts, RNA editing may subtly effect the stability of the RNA molecule which in the end would effect expression.
Mattick links alu sequences to the function of memory formation in the human brain. He points out that the ADAR2 protein which is involved in RNA editing binds to alu sequences. ADAR2 is linked to cell signaling pathways involved in memory formation. Mattick believes that this may be a way that an organisms environment and an individual's experiences can shape the way memories are formed.
Gommans and Maas describe RNA editing in terms of evolvability. They argue that selection may favor systems with high levels of diversity and that the drive toward complexity may arise from the need to keep selfish elements under control. They argue that the more complex an organism is, the more resilient it is against the effects of RNA editing. This inevitably leads to tolerance and proliferation of alus that induce RNA editing. This new editing increases the complexity of the organism even more which results in a feedback loop of ascending complexity.
The debate about how much of the noncoding genome is functional is fundamentally misguided. In the case of transposable elements in general and alus in particular, all are in some sense evolutionarily successful or they would not be there at all. But are they functional? I suppose it depends on your perspective. I am reminded of Lane's musings on the troubled birth of the individual. While they generally share the same interests, even the cells in our own body cannot cooperate without mechanisms in place to force them into compliance. All of the genes and other elements in the genome also have a strong incentive to cooperate because if the organism dies then none of them are passed on. But, all elements in the genome must balance these common interests with their own individual interests and unlike rebellious cancerous cells which will never break free, selfish genetic elements are free to evolve and explore ways to pass themselves on. To survive, all elements in the genome must find ways to pass themselves on. So, if a transposable element is recruited by natural selection to perform some function, this element has not lost some kind of battle. From it's perspective, this is the best thing that can happen as being recruited to a task grants the element job security. The same thing happens when a protein coding gene is duplicated. The newly spawned gene must contribute something useful or risk being thrown out by natural selection. Whether you think of the individual in terms of a colony of cells or a group of genes, nothing noteworthy, beautiful or complex can arise without some kind of conflict among the constituent parts. Natural selection does not just magically push life toward complexity. Conflict in the genome isn't about "parasitic" sequences "invading" the genome. Rather, it is about millions of elements cooperating, if reluctantly, to form a cohesive whole. Without conflict, natural selection would have nothing to work with at all.
Monday, March 15, 2010
Did we evolve to evolve?
As I discussed in previous posts, ALU elements are unique to primates and the fact that their proliferation rates and transcription patterns are different in humans than other primates suggests that they may be responsible some uniquely human traits. In "Under The Genomic Radar: The stealth model of alu amplification" Han and Xing, put forward some ideas about why some subfamilies of ALUs suddenly proliferate after millions of years with no activity. They explain that the AluYa and AluYb alu subfamilies actually date back 18-26my. However, the proliferation of these sequences has only occurred in the human lineage. Since the parent sequences date much further back in the primate genome, it seems that the capacity for proliferation has been there for quite some time.
The traditional model has been that master ALU sequence continually spawns daughter sequences that proliferate throughout the genome. However, this simplistic model fails to account for the fact that proliferation rates vary widely over time and across taxa. Han and Xing explain their stealth driver model as an alternate explanation. They believe that a low activity sequence can lurk in the genome over long periods of time. Occasionally, this sequence may spawn a daughter sequence that is much more active, these daughter sequences are actually responsible for the vast majority of the activity.
These highly active daughter sequences are highly likely to be detrimental to the organism. Natural selection may weed these out, but the parent stealth driver would be invisible to natural selection so it would be allowed to persist to spawn another high activity daughter sequence in the future.
In this sense, ALU elements themselves have in fact evolved to evolve. However, there is no reason to think that they have our interests in mind. These stealth drivers lay low because they don't want to kill their hosts and end up dead themselves. But, if they lay low forever they will be drowned out by their competitors.
But when do they come out of their hiding place? According to Hedges in "Differential alu mobilization and polymorphism among human and chimp lineages" it may be that these sequences end up proliferating when natural selection is unable to weed them out. This would occur during a population bottleneck. I found this idea very intriguing because as Wray pointed out in my last post, some uniquely human characteristics may be regulated by ALU transcription in the human brain. For example, regulation of the prodynorphin gene which has roles in memory, emotional status and perception. If Hedges idea is true, then a population bottleneck 3 million years ago could have been responsible for the fact that certain subfamilies that have not expanded in other primate lineages ended up proliferating in the human lineage. Hedges explains that any deleterious ALU insertion would be selected out by natural selection. But, in a population bottleneck, natural selection may not be able to get rid of the high activity master ALU sequence itself. So, although deleterious changes would be weeded out as they appear, the sequences would continue to proliferate. The vast majority of those that persist would be either neutral or very slightly deleterious. The human lineage is known for its bushiness. This extra variation may have driven increased speciation events. Is it possible that these extra raw materials may have given rise to some unique human traits? I believe the answer might be yes.
I have a lot more on my list to read on this topic. My research has led to some papers coming from the U which is pretty cool. My goal is to shed some light on the unique path that human evolution has trod and perhaps show that whether or not it is always beneficial to the organism as a whole, selfish elements in our genome have evolved to evolve. Perhaps the friction among these rival elements are the spark that ignited human evolution.
The traditional model has been that master ALU sequence continually spawns daughter sequences that proliferate throughout the genome. However, this simplistic model fails to account for the fact that proliferation rates vary widely over time and across taxa. Han and Xing explain their stealth driver model as an alternate explanation. They believe that a low activity sequence can lurk in the genome over long periods of time. Occasionally, this sequence may spawn a daughter sequence that is much more active, these daughter sequences are actually responsible for the vast majority of the activity.
These highly active daughter sequences are highly likely to be detrimental to the organism. Natural selection may weed these out, but the parent stealth driver would be invisible to natural selection so it would be allowed to persist to spawn another high activity daughter sequence in the future.
In this sense, ALU elements themselves have in fact evolved to evolve. However, there is no reason to think that they have our interests in mind. These stealth drivers lay low because they don't want to kill their hosts and end up dead themselves. But, if they lay low forever they will be drowned out by their competitors.
But when do they come out of their hiding place? According to Hedges in "Differential alu mobilization and polymorphism among human and chimp lineages" it may be that these sequences end up proliferating when natural selection is unable to weed them out. This would occur during a population bottleneck. I found this idea very intriguing because as Wray pointed out in my last post, some uniquely human characteristics may be regulated by ALU transcription in the human brain. For example, regulation of the prodynorphin gene which has roles in memory, emotional status and perception. If Hedges idea is true, then a population bottleneck 3 million years ago could have been responsible for the fact that certain subfamilies that have not expanded in other primate lineages ended up proliferating in the human lineage. Hedges explains that any deleterious ALU insertion would be selected out by natural selection. But, in a population bottleneck, natural selection may not be able to get rid of the high activity master ALU sequence itself. So, although deleterious changes would be weeded out as they appear, the sequences would continue to proliferate. The vast majority of those that persist would be either neutral or very slightly deleterious. The human lineage is known for its bushiness. This extra variation may have driven increased speciation events. Is it possible that these extra raw materials may have given rise to some unique human traits? I believe the answer might be yes.
I have a lot more on my list to read on this topic. My research has led to some papers coming from the U which is pretty cool. My goal is to shed some light on the unique path that human evolution has trod and perhaps show that whether or not it is always beneficial to the organism as a whole, selfish elements in our genome have evolved to evolve. Perhaps the friction among these rival elements are the spark that ignited human evolution.
Monday, March 8, 2010
ALU elements and human evolution
One of the most exciting areas around noncoding sequences are the discoveries being made around ALU elements expressed in the brain. This article is a good review of the current research. A 2006 paper by Hasler and Strub "ALU elements as regulators of gene expression" in the journal Nucleic Acids Research explains that ALU elements arose exclusively in the primate lineage and are implicated in shaping the evolution of the primate brain.
ALUs have been shown to be involved in alternative splicing. They have also been shown to edit mRNAs in other ways as well. The paper talks about a process called exonization where a previously intronic sequence is recruited into the coding region of a gene. When this area includes an ALU element, there is potential for this exon to be alternatively spliced. Computational studies have confirmed that this does indeed happen.
Since ALUs evolved very recently, they all share much similarity. This makes it easier to do bioinformatic studies on them. Also, the fact that they are exclusive to the primate lineage is exciting because they may be the secret that sets humans apart.
ALUs have been shown to be involved in alternative splicing. They have also been shown to edit mRNAs in other ways as well. The paper talks about a process called exonization where a previously intronic sequence is recruited into the coding region of a gene. When this area includes an ALU element, there is potential for this exon to be alternatively spliced. Computational studies have confirmed that this does indeed happen.
Since ALUs evolved very recently, they all share much similarity. This makes it easier to do bioinformatic studies on them. Also, the fact that they are exclusive to the primate lineage is exciting because they may be the secret that sets humans apart.
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