TEs and Macroevolution

I'm going to discuss two papers that were recently released electronically by the journal BioEssays, both having to do with TEs and macroevolution. The first, by Oliver and Greene (2009), came to my attention last month when I read a horrible press release that has become the norm in science journalism these days. I recently got my hands on the paper in question and after reading it was relieved to see it wasn't nearly as bad as I thought it was going to be. However, it certainly wasn't the earth-shattering, paradigm-shifting, gift from the heavens for evolutionary biology that the press release made it out to be. It did however elaborate on and articulate some interesting ideas that have only been mentioned briefly, if at all, in the TE literature.

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.