Friday, June 24, 2011
Long time no see. This blog has suffered from a phase of no posts due to several reasons, namely being a long period of laziness and then the stress of having to write my Masters thesis and defend it. So I hope you'll forgive me, because I would really like to get back into doing this. Even if few people read it, in the least it would be good writing practice.
What has shaken me from my blog post-less slumber? A number of months ago I heard somewhere that a new TE book was going to be coming out, which is a rare event and welcome since the number of TE-related books is quite small. I decided more or less on the spot that I would review it on the blog when I finished reading it.
The book in question, Mobile DNA Finding Treasure in Junk, was written by noted human L1 retrotransposon researcher Dr. Haig Kazazian Jr currently at Johns Hopkins University School of Medicine. The Kazazian Lab has been one of the premiere L1 research labs for the last 20 years and has made many great discoveries into the biology of L1 elements and non-LTR retrotransposons in general.
I more or less enjoyed the book, although for different reasons than I thought I would have originally, and it was a rather quick read, for me at least, clocking in at around 3 or 4 hours which I managed to do yesterday evening. I was expecting a broad overview of TE biology and perhaps the history of their discovery and characterization but it wasn't quite that. There were a few introductory chapters on basic TE biology, and a very brief summary of their discovery and some of the major researchers in the field. A lot of the opening chapters felt a little scattershot, with not a great deal connecting them besides they unifying fact they were all about TEs. I think they would have been fine there had been a little more depth in the chapters, but ah well. The next part of the book is essentially the history of L1 research in the Kazazian Lab, which is a bit jarring at first and quite a departure from the format at the start of the book but this is where the most interesting material lies. It's always nice to see the more human and nitty-gritty part of research that you never get reading the primary literature. Learning a bit more about the people behind the author lists on papers is always quite cool, I find. And although I never expressed interest in learning about the behind the scenes of L1 research before I found it hard to put the book down during this section. For example, I've been seeing the terms LINEs and SINEs for years, since undergrad, but never once wondered who actually coined the two terms. It actually turned out to be Maxine Singer, one of the pioneering L1 researchers and someone who was instrumental in introducing Kazazian to them. The personal touches reminded me a little of Esra Galuns book on TEs that I read a few years back which I enjoyed. So for those interested in the human side of research, and those who are dying to know about the history of L1 this book is not too shabby.
One of the things I found problematic with this book was it's treatment, or rather lack thereof, of the selfish DNA hypothesis. I find it hard to imagine writing a modern book about TEs without going into Selfish DNA at least a little bit but this book manages to do that. Although one of the selfish DNA papers is cited (Orgel and Crick but not Doolittle and Sapienza), it is cited as the source for the term 'junk DNA ', which was actually coined by Susumu Ohno. Not only this but in another paper several years later Doolittle (1982) responded to critics by arguing that junk and Selfish DNA are not synonyms and should not be used as such. I don't think I have ever seen this latter 1982 paper cited, and the confusion between junk and selfish DNA is a common one in the TE literature unfortunately.
Near the end of the book, Kazazian waxes about the prevalence of TEs in genomes and falls into that familiar trap of " if TEs are so prevalent, abundant and persistent in genomes it's hard to imagine they aren't performing some beneficial function". This is where I think it is so crucial, nay, essential, to come at transposon biology from a evolutionary perspective because to me it makes understanding and interpreting TEs so much more tractable. I don't argue that sometimes TE-derived sequence have provided benefit to host organisms, by this point it's a foregone conclusion (see Feschotte and Pritham, 2007; Feschotte, 2008 and Sinzelle et al., 2009 for numerous examples). What I do argue is that most TEs in genomes provide no benefit and persist due to a combination of intra-genomic selection, antagonistic co-evolution with their host and other TEs and genetic drift due to the low effective population sizes of many eukaryotic organisms.
In conclusion, not a great book if you want an overview of TE biology, for that I'd recommend picking up and reading some key papers, but if you are interested in some of the behind the scenes of the history of L1 research, than this book is for you.
Ohno, S. 1972. So much "junk" DNA in our genome. In Evolution of Genetic Systems (ed. H.H. Smith), pp. 366-370. Gordan and Breach, New York
Doolittle, W.F. and C. Sapienza. 1980. Selfish genes, the phenotype paradigm and genome evolution. Nature 284: 601-603
Orgel, L.E. and F.H.C. Crick. 1980. Selfish DNA: the ultimate parasite. Nature 284: 604-607
Doolittle, W.F. 1982. Selfish DNA after Fourteen Months. In Genome Evolution (eds. G.A. Dover and R.B. Flavell), pp. 3-28. Academic Press, London
Feschotte, C. and E.J. Pritham. 2007. DNA transposons and the evolution of eukaryotic genomes. Annual Review of Genetics 41: 331-368
Feschotte, C. 2008. Transposable elements and the evolution of regulatory networks. Nature Reviews Genetics 9: 397-405
Sinzelle, L., Z. Izsvák, and Z. Ivics. 2009. Molecular domestication of transposable elements: From detrimental parasites to useful host genes. Cellular and Molecular Life Sciences 66: 1073-1093
Tuesday, November 3, 2009
Figure 1. Sizes are relative and not to scale. UTR-untranslated region; APE-apurinic/apyrimidinic endonuclease;RT-reverse transcriptase; RNH-RNase H
This weeks entry deals with several inter-related retrotransposons from the rice blast fungus Magnaporthe grisea, a pathogenic fungus which infects not only rice but other species of plants. Many of the retrotransposons, and DNA transposons, from M. grisea were discovered when researchers were trying to determine the molecular reasons for it's resistance to certain biological counter-measures produced by the plants it infects. Often this was caused by the insertion of various TEs into so-called avirulence genes in the M. grisea genome.
Two SINEs (Short Interspersed Elements) from M. grisea were characterized in 1995, Mg-SINE and Ch-SINE ( Kachroo et al., 1995). The former is around 472 bp long, has a tRNA-derived 5' end and it's 3' end is 99% similar to the 3' end of the LINE element MGL from the same species (Thon et al., 2004). The latter also have a 3' end very similar to MGL which indicates that both SINEs are probably reverse transcribed and inserted into the genome by the proteins MGL encodes (Okada et al., 1997).
So far this story isn't too weird( <---- inadvertent foreshadowing, I swear) because LINE-SINE pairs have been found many times in different genomes. Where it does get weird is with an element discovered several years later named MINE ( Fudal et al., 2005). MINE consists of a non-coding sequence at the 5' end termed WEIRD fused to various 5' truncated MGL elements. Some ~30 individual loci were found, nearly all of which had different truncated MGL elements fused to the standard WEIRD sequence which never varied. How do fusions like this occur you might ask? Well, they are typically thought to occur through a process known as template jumping. A retrotransposon replicates by making a complementary DNA, or cDNA, copy of it's RNA using the reverse transcriptase it encodes. During this process the reverse transcriptase can sometimes jump from one RNA template to another and keep on copying, effectively making a cDNA which is a fusion or chimera of several different RNA templates. If while an MGL element was creating a cDNA itself a WEIRD RNA was close by, the RT could jump from the MGL to the WEIRD and create the fusion product. This gets integrated back into the genome because it has the special sequence of the MGL 3' end and voila, you have a MINE insertion.
The most interesting thing about MINE is the fact that there are so many insertions that seemed to have come from independent template jumping events. Some of the MINE insertions were of the same copy but most of them had unique 5' truncated MGL sequences at their 3'ends, suggesting that for whatever reason this WEIRD sequence keeps getting fused to MGL again, and again and again. They found at least 30 instances of this.
The authors describe finding expressed sequence tags, or ESTs, of WEIRD and MINE elements in the EST database for M. grisea. Basically this means that WEIRD and some MINEs are actually being expressed, like genes would be, by the M. grisea genome. What they couldn't find however were any WEIRD sequences on their own, but this may have been due to the fact that the genome sequence data wasn't complete yet (Gogvadze et al., 2007). They found WEIRD transcripts mainly in cells during the process of infecting a host suggesting that this WEIRD sequence might actually be a functionally important RNA for the fungus. Wherever this WEIRD is coming from it seems that it either has a very high propensity for being fused to MGL or it is present in such high concentrations that the creation of these MINE insertions is very common. Gogvadze et al. also found two other insertion that were due to template jumping composed of, respectively, a WEIRD-Mg-SINE-MGL fusion and a WEIRD-Mg-SINE fusion.
Unlike other instances of template jumping, where the point in the non-LTR sequence where the new sequence begins, in MGL the authors appear to have identified jumping hot spots. They found a preponderance of WEIRD sequences joining MGL sequences near predicted hairpin structures in the MGL mRNA (Gogvadze et al., 2007). They thought that these hairpins might be acting like blocks which stall the RT enzyme just enough so that another template like WEIRD can sneak in.
What interest me about this system is the number of independent fusion events that ocurred. We could be seeing something analogous to the initial formative steps of something like a new SINE, although we can't exactly call it a Short Interspersed Element, and Long Interspersed is already taken :P If certain insertions can make full-length transcripts and can continue to parasitize the proteins of MGL with enough frequency and efficiency it very well could be.
Fudal, I., H.U. Böhnert, D. Tharreau, and M.-H. Lebrun. 2005. Transposition of MINE, a composite retrotransposon, in the avirulence gene ACE1 of the rice blast fungus Magnaporthe grisea. Fungal Genetics and Biology 42: 761-772.
Gogvadze, E., C. Barbisan, M.-H. Lebrun, and A. Buzdin. 2007. Tripartite chimeric pseudogene from the genome of rice blast fungus Magnaporthe grisea suggests double template jumps during long interspersed nuclear element (LINE) reverse transcription. BMC Genomics 8: 10.1186/1471-2164-1188-1360.
Kachroo, P., S.A. Leong, and B.B. Chattoo. 1995. Mg-SINE: A short interspersed nuclear element from the rice blast fungus, Magnaporthe grisea. Proceedings of the National Academy of Sciences of the United States of America 92: 11125-11129.
Okada, N., M. Hamada, I. Ogiwara, and K. Oshima. 1997. SINEs and LINEs share common 3' sequences: a review. Gene 205: 229-243.
Thon, M.R., S.L. Martin, S. Goff, R.A. Wing, and R.A. Dean. 2004. BAC end sequences and a physical map reveal transposable element content and clustering patterns in the genome of Magnaporthe grisea. Fungal Genetics and Biology 41: 657-666.
Monday, October 5, 2009
The lack of posts lately has been due to several things: lab work, laziness, having to input and organize my collection of literature into a new program, and trying to find certain references so I can do my Selfish DNA posts in the (almost) correct chronological order. The labwork remains, as always, the laziness has subsided somewhat, all of the literature I've read has been inputted into Mendeley, and I finally think I've reached the very first mention of selfish DNA in the literature.
This is an oldie, but a goodie is seems.
While not talking about transposable elements I do feel that this is one of those papers that every transposon biologist should be required to read. I'll probably say that about every piece of literature featured in these Selfish DNA posts but, nonetheless. Östergren's paper deals with the presence of extra, or B, chromosomes in plants. B chromosomes are superfluous chromosomes found in a number of different taxa that have acquired through mutation a means of ensuring that they are passed down to offspring even if they are not essential for survival. These chromosomes were the first kind of selfish DNA to be discovered but it was this paper, to the best of my knowledge, that first proposed that they were molecular parasites.
Östergren does consider that they could be beneficial but then proposes what most would assume to be is favourable alternative:
"Selection brings about an increase in frequency of favourable genes and chromosomes. In the case of the normal complement the chromosomes cannot have a positive selection value except by being favourable to the individuals carrying them. The differential behaviour of the extra fragments, however, makes their 'response' to selection quite different from that of the normal complement. If there occurred a constitutional variation in their mechanism of differential behaviour (their accumulation mechanisms) caused by structural or mutational changes within them, selection would accumulate such fragments as have the most efficient power of spreading, even if they were quite neutral in effect on the plant or even unfavourable....The decisive point in the selection of fragments with a differential behaviour is how favourable their properties are for their own existence rather than how favourable they are to the plant."
And there we have the first articulation of the selfish DNA hypothesis, over thirty years before Dawkins published The Selfish Gene. It's amazing what you can find in some of the older literature. I myself was rather surprised at some of the things Östergren articulates in this paper. He was really ahead of his time. Or we're behind in ours :P
He touches on the seemingly inevitable Red Queen molecular arms race that must occur between selfish DNA and its host:
"The relation between such extra fragments and their carrying plants obviously bears a strong resemblance to the relation between a parasite and its host. Selection will favour such changes in the parasite as give it an increased power of spreading from host to host. On the other hand, selection will also favour such changes in the host as enable it to get rid of the parasite. A similar antagonism...should be expected between parasitic fragment chromosomes and the plants carrying them."
He also makes the crucial parallel between parasitic organisms and selfish DNA which I think is one of the most important things to keep in mind when thinking about any selfish genetic elements. To me, so many bad interpretations have arisen because people tend to forget things like transposable elements are, to a certain extent, separate evolutionary entities from their host.
Östergren mentions one final thing that was once again ahead of his time but I think I'm going to save that for a future non-Selfish DNA post.
Östergren, G. 1945. Parasitic nature of extra fragment chromosomes. Botaniska Notiser 2: 157-163.
Tuesday, July 21, 2009
Cassandra elements are non-autonomous LTR retrotransposons that were identified in several species of angiosperm plants and ferns (Kalendar et al., 2008). Cassandras are part of of category of non-autonomous LTR elements known as TRIMs (terminal repeat retrotransposon in miniature) which possess the characteristic flanking long terminal repeats (LTRs) on either side of a small core sequence which encodes none of the proteins typically seen in LTR elements (Witte et al., 2001). TRIMs, like Cassandra, are thought to retrotranspose by parasitizing the various proteins of autonomous LTR elements by competing with autonomous transcripts. What makes Cassandra different is that it has a 5S rRNA gene inserted into both of its LTRs.
LTRs contain the regulatory sequences important for transcription of LTR-bearing retroelements, including retroviruses and ERVs, and normally LTR retrotransposons have RNA polymerase II promoters in their LTRs to get the job done. However, Cassandra appears to be using the endogenous RNA polymerase III promoter at the 5' end of the inserted 5S rRNA instead. Analysis of the 5S rRNA sequence also suggested that it might under selective restraint, possibly allowing Cassandra to better bind to transcription factor II proteins to initiate transcription more easily or to take advantage of the paucity of methylation that occurs in normal 5S rRNA promoters, allowing Cassandra to escape suppression by the host genome.
How did the 5S rRNA get there though? The authors hypothesize that long ago ( around 270 million years ago at least based on the phylogenetic distribution of Cassandra) a 5s rRNA-derived SINE (short interspersed nuclear element, a non-autonomous non-LTR retrotransposon) inserted into the LTR of a proto-Cassandra element. This insertion may have conferred a selective advantage on that element, for aforementioned reasons, and allowed it to flourish.
So we have a parasite ( a 5s rRNA-derived SINE) of a parasite ( a non-LTR retrotransposon) inserting into a parasite (TRIM) of another parasite (autonomous LTR retrotransposon) and subsequently being exapted for a new function.
Kalendar, R., J. Tanskanen, W. Chang, K. Antonius, H. Sela, O. Peleg, and A.H. Schulman. 2008. Cassandra retrotransposons carry independently transcribed 5S RNA. Proceedings of the National Academy of Sciences of the United States of America 105: 5833-5838.
Witte, C., Q.H. Le, T. Bureau, and A. Kumar. 2001. Terminal-repeat retrotransposons in miniature (TRIM) are involved in restructuring plant genomes. Proceedings of the National Academy of Sciences of the United States of America 98: 13778-13783.
Sunday, July 12, 2009
The origins of the selfish DNA hypothesis, later elaborated by Orgel and Crick and Doolittle and Sapienza (1980; both to be covered in a future post), reside in one of the more popular books written by Richard Dawkins The Selfish Gene. For those who haven't read it the book is essentially Dawkins' treatise on how he feels the sole units of evolution are genes and most of everything else is just an extrapolation from this level. Although I disagree with Dawkins' assertion that genes are the fundamental units and targets of selection I do recognize that he was the first to propose that the copious amounts of seemingly superfluous DNA found within metazoan genomes could be explained using his selfish gene theory.
In his own words, from the 30th anniversary edition of the book, pages 44-45:
"Sex is not the only apparent paradox that becomes less puzzling the moment we learn to think in selfish gene terms. For instance, it appears that the amount of DNA in organisms is more than is strictly necessary for building them: a large fraction of the DNA is never translated into protein. From the point of view of the individual this seems paradoxical. If the 'purpose' of DNA is to supervise the building of bodies it is surprising to find a large quantity of DNA which does no such thing. Biologists are racking their brains trying to think what useful task this apparently surplus DNA is doing. From the point of view of the selfish genes themselves, there is no paradox. The true 'purpose' of DNA is to survive, no more and no less. The simplest way to explain the surplus DNA is to suppose that it is a parasite, or at best a harmless but useless passenger, hitching a ride in the survival machines created by the other DNA."
Only a few sentences but they would be the beginning of what was to come next in 1980. More on that in the next post.
P.S. Sorry that this is so short, stay tuned.
Monday, June 22, 2009
Today’s post is another article summary but about something a bit different. This one concerns the origins of adaptive immunity in jawed vertebrates, and more specifically the origin of the RAG1 protein. RAG1 is a gene expressed in T and B-lymphocytes in the immune system which along with RAG2 mediates the creation antibodies. It does this via a process known as V(D)J recombination, after the variable and joining sequence segments that are joined together to create a complete antibody gene. The RAG1/2 complex binds to recognition signal sequences (RSS) between segments and cuts out the intervening DNA. The subsequent double-strand breaks are joined back together via non-homologous end-joining proteins to join the previously separated sequence into a single coding region. This is an oversimplification of the process but basically this occurs several times in a somewhat random manner to create a novel antibody gene. Through a selection process that occurs in the immune system only cells with antibodies which recognize foreign antigens survive to prevent autoimmunity.
Researchers noticed some time ago that the process of V(D)J recombination was very similar to what occurs during the transposition of a Class II TE, also known as a DNA transposon. A transposase protein recognizes and binds to the inverted terminal repeats (ITR) on either end of the element and cuts it out of the sequence it is inserted into. In a similar manner RAG1/2 complexes bind to a pair of RSS’s, cut out the sequence in between and circularize it for degradation by the cell. In 2005 Kapitonov and Jurka published a paper showing that roughly 60 amino acids in the C-terminus of RAG1, within the so-called “RAG core”, were found to be significantly similar to the Transib transposases. As well, the ITRs of Transib elements are very similar to the RSS’s (with a probability of the similarity occurring by chance of 1.0 x 10-3) and both RAG complexes and Transib elements generate 5 bp target site duplications (TSD). It seemed like the origin of RAG1 had been at least partially solved.
Several weeks ago a paper popped up in my iGoogle Reader that has been published in PLoS One contesting the transposon origin of RAG. This seemed odd to me because I thought the conclusions of Kapitonov and Jurka (2005) were pretty sound. The paper by Dreyfus (2009) claimed that there was more evidence that RAG1 was derived from the insertion of a herpes virus-like element long ago in a deuterostome ancestor. You can judge for yourself, the paper is available free to download here, but I’d like to tell you why this new hypothesis doesn’t hold up as well to me as the Transib origin one does.
Dreyfus states that the regulatory sequences of the Epstein-Barr Virus (EBV), a herpes virus, are very similar, identical in some cases, to the regulatory sequences possessed by RAG1. He also cites the fact that EBV infections activate the expression of RAG1/2 and that when the virus excises from host DNA it forms a circle, much in the same way intervening sequences form circular intermediates during V(D)J recombination. And both RAG1 and the ICP-8 protein of EBV have DDE metal ion binding motifs important for cleavage of target DNA despite the fact they do not possess any significant primary sequence identity. Dreyfus says that despite the sequence similarity between the RAG1 core and Transib transposases there is the problem of the RAG1 amino terminus which is not similar. He also states that during the evolution of the proto-RAG1 there would be no selective benefit to the expression of a Transib element in proto-immune cells and that the antigenic effects of some herpes-virus proteins would provide a reason for the selective maintenance of an inserted herpes-like element. Also, no autonomous “RAG transposon” has been found in nature yet and neither has an element been found encoding a RAG2 homolog which is required for V(D)J recombination to occur.
The regulatory similarities between EBV and RAG1 are interesting but I think the answer as to the probable origin of RAG is pretty clear. The fact that both ICP-8 and RAG1 possess the DDE catalytic motif is not evidence of common ancestry as this motif evolved multiple times independently in several DNA transposon superfamilies, including Transib, and in proteins like RNase H and the Argonaute component of RISC. DNA transposons forming circles as intermediates is not unknown and a good example I read of recently are the TEs in ciliates that seem to be involved in the drastic chromosomal rearrangement of those species. Dreyfus did not put any sequence alignment diagrams in his paper because ICP-8 and RAG1 could not be aligned while Kapitonov and Jurka (2005) were able to align the Transib transposase and RAG1 and show their significant similarity. The so-called “ amino terminus problem” really isn’t a problem at all because last year Panchin and Moroz (2008) published a paper where they found a Chapaev superfamily DNA transposon, N-RAG, from the mollusc Aplysia californica whose transposase had significant similarity to the “ problematic” N terminus of RAG1. This paper is not cited by Dreyfus. It turns out RAG1 might actually be derived from two separate DNA transposons, not just one. As for the maintenance problem because TEs are selfish and can proliferate even at a fitness cost to the host there really is no need to explain why the proto-RAG1 transposon could persist.
The story is not over for RAG1 though. I agree with Dreyfus that the issue of where the RAG2 gene came from needs to be addressed as well as trying to flesh exactly how the evolutionary process proceeded from an autonomous DNA transposon to modern day RAG.
Dreyfus, D.H. 2009. Paleo-immunology: evidence consistent with insertion of a primordial herpes virus-like element in the origins of acquired immunity. PLoS One 4: e5778.
Kapitonov, V.V. and J. Jurka. 2005. RAG1 core and V(D)J recombination signal sequences were derived from Transib transposons. PLoS Biology 3: e181.
Panchin, Y. and L.L. Moroz. 2008. Molluscan mobile elements similar to the vertebrate Recombination-Activating Genes. Biochemical and Biophysical Research Communications 369: 818-823.
Friday, June 12, 2009
First they detail the effects TE can have on organisms and species by the varied and numerous kinds of mutations they can cause which introduce variability. Next they briefly discuss that the mutagenic potential of TEs might be harmful to the individual but at the population and species level this could actually translate into a higher capacity to evolve via greater variability. Basically they are mentioning a form of multi-level selection. In theory, lineages with TEs which are actively causing new mutations through insertions, ectopic recombination and other mechanisms will have higher genetic variability than those whose TEs are mostly inactive or suppressed.
Examples of this might be things like the tuatara or the coelacanth ,whose genomes are either composed of little TE DNA or their elements have been silenced either through host-level selection or through stochastic events at the level of both the host and the elements. The authors also discuss the activity of TEs in the germline and the regulatory changes that can take place due to this activity through TEs perturbing methylation and chromatin patterns. Stress induced TE activity is also mentioned as well as the fact that one of the few examples of an organism that has almost completely reigned in it's TEs, the fungus Neurospora crassa via repeat-induced point mutation, has also crippled it's ability to evolve new genes by gene duplication because these are recognized in the same manner as TEs and mutated into oblivion.
Overall I found this paper interesting but there were a few notable flaws. In the discussion about N. crassa and its apparent evolutionary disadvantage by mutating multi-copy DNA the authors seem to imply that other species allow TEs to be active because this is selectively beneficial at higher levels. Evolution does not work this way. Selection at the host-level would never favour any mutations which allowed TEs to be active simply because the variation they cause could be beneficial to the lineage or group that species belongs to. TEs and the host genomes they inhabit are locked in a co-evolutionary arms race where selective pressures on the TEs favour elements which can slip free of the suppressive bonds the host imposes on them, while in turn pressure at the level of the host favours individuals who can suppress TEs as effectively and efficiently as is possible. TEs are never allowed to transpose. Any species which allowed TEs to transpose probably does not exist anymore because it went extinct, along with its complement of elements. Similarly, they talk of TEs being permitted to transpose in the germline where they will do the least harm to the organism and contribute to genetic variation. I don't think they did this intentionally but it weakens their overall argument when they lapse into explanations such as these. They also fall into the classic " looks like TEs aren't junk DNA after all" trap and refer to them as "helpful parasites" several times throughout the paper. To repeat again: no species keep TEs around because they are beneficial. While it could be true that lineages which possess active TEs have a greater capacity for evolvability, it is next to impossible that TEs are maintained by host-level selection for their variation inducing qualities. You don't need to invoke that to explain the presence of TEs.
The second paper is along the same lines and expands upon something that was brought up by Oliver and Green. Zeh et al. (2009) deals with punctuated equilibria, TEs and the epigenetic alterations they can cause. Epigenetics is basically gene regulation but in the paper what the authors mean is things like methylation patterns, chromatin remodelling and RNA interference, or the more recently popularized and charismatic forms of gene regulation. The heart of this paper is the “epi-transposon hypothesis” put forth by the authors as an explanation for the punctuated evolutionary events often seen in the fossil record:
1) TEs become active during stressful events such as the colonization of new habitats or climate change etc.
2) TE activity causes mutations via disruptive insertions, chromosomal rearrangements, epigenetic alterations etc.
3) These mutations can push a species out of a local adaptive peak into another higher one in a short period of time
The authors propose that during periods of stasis TEs are kept relatively silent by epigenetic silencing and other control mechanisms of the host. Stress or the invasion of a new habitat perturbs these controls, TEs run wild and muck things up and can cause these punctuated events that can lead to rapid speciation. They cite several examples of bursts of TE activity coinciding with the diversification of various taxa such as haplochromid cichlids, mammals in general and bats.
I think they are right that bursts of TE activity could be contributing to punctuated events, in conjunction with the isolation of populations. The question is the frequency with which punctuated events are generated by TEs and not something like polyploidy. Seeing this paper and writing this blog post also prompted me to actually go read the gigantic Eldredge and Gould paper of 1972 where they explain punctuated equilbria.
These are both important papers in the sense that they are potentially bringing these sorts of issues to the attention of the TE community at large. It would just be nice if they weren’t tied to horrendous press releases and tired and incorrect statements about how because some TE mutations might be beneficial this means they aren’t selfish or junk. Maybe someday.
Oilver, K.R. and W.K. Greene. 2009. Transposable elements: powerful facilitators of evolution. BioEssays: DOI 10.1002/bies.200800219.
Zeh, D.W., J.A. Zeh, and Y. Ishida. 2009. Transposable elements and an epigenetic basis for punctuated equilibria. BioEssays: DOI 10.1002/bies.200900026.