Cover Image

HARDBACK
$89.75



View/Hide Left Panel

is that SGEs lead to antagonistic co-evolution with other components of the genome. Important features of eukaryotic genomes (e.g., DNA methylation, RNAi, small RNA regulatory pathways, R-M systems) have evolved, at least in part, as defense mechanisms against SGEs. Many genetic elements have mixed phenotypes, with both selfish (parasitic) and “beneficial” (“mutualistic”) features. The classic example is the mitochondrion, which is clearly beneficial but also shows selfish features (e.g., cytoplasmic male sterility) that reduce nuclear gene fitness, thus leading to genetic conflict. Evolutionary dependency can also evolve in hosts with ubiquitous SGEs, which can lead to irreversible dependence. Growing evidence supports a significant role of SGEs in eukaryotic development and speciation, and possibly also in extinction of species. Genome domestication of SGEs leads to evolutionary innovations, including acquisition of new genes and gene regulation from TEs, heritable microbes (e.g., Wolbachia), and selfish plasmids. Safe havens can promote longer associations of SGEs with host lineages and also may facilitate their domestication. Finally, distinctions are made between the evolutionary consequences of SGEs and the factors that maintain them over evolutionary time. Clear formulations of the idea of evolvability as a means for evolutionary maintenance of SGEs will facilitate rigorous testing of this idea. Nevertheless, current evidence strongly supports the view that SGEs are maintained by their transmission-enhancing phenotypes and that evolutionary innovations emerging from them are a consequence of their existence rather than the cause.

ACKNOWLEDGMENTS

I thank J. Strassmann, D. Queller, J. Avise, and F. Ayala for organizing In the Light of Evolution V: Cooperation; and A. Avery, R. Edwards, T. Eickbush, C. Feschotte, D. Loehlin, M. Clark, J. Jaenike, M. Lenoe, C. Landry, R. Minckley, P. Nagarajan, and D. Wheeler for assistance and comments on the manuscript. Because of space limitations, topic reviews are sometimes cited in lieu of the original research paper and the reader is encouraged to access the reviews for primary research sources. Support for this work came from National Science Foundation Grants DEB0821936 and NIH GM084917.



The National Academies | 500 Fifth St. N.W. | Washington, D.C. 20001
Copyright © National Academy of Sciences. All rights reserved.
Terms of Use and Privacy Statement