Selfish genetic element

Selfish genetic elements (historically also referred to as selfish genes, ultra-selfish genes, selfish DNA, parasitic DNA and genomic outlaws) are genetic segments that can enhance their own transmission at the expense of other genes in the genome, even if this has no positive or a net negative effect on organismal fitness.[1][2][3][4][5][6] Genomes have traditionally been viewed as cohesive units, with genes acting together to improve the fitness of the organism. However, when genes have some control over their own transmission, the rules can change, and so just like all social groups, genomes are vulnerable to selfish behaviour by their parts.

Early observations of selfish genetic elements were made almost a century ago, but the topic did not get widespread attention until several decades later. Inspired by the gene-centred views of evolution popularized by George Williams[7] and Richard Dawkins,[8] two papers were published back-to-back in Nature in 1980 – by Leslie Orgel and Francis Crick[9] and by Ford Doolittle and Carmen Sapienza[10] – introducing the concept of selfish genetic elements (at the time called "selfish DNA") to the wider scientific community. Both papers emphasized that genes can spread in a population regardless of their effect on organismal fitness as long as they have a transmission advantage.

Selfish genetic elements have now been described in most groups of organisms, and they demonstrate a remarkable diversity in the ways by which they promote their own transmission.[11] Though long dismissed as genetic curiosities, with little relevance for evolution, they are now recognized to affect a wide swath of biological processes, ranging from genome size and architecture to speciation.[12]

  1. ^ Werren JH, Nur U, Wu CI (November 1988). "Selfish genetic elements". Trends in Ecology & Evolution. 3 (11): 297–302. doi:10.1016/0169-5347(88)90105-x. PMID 21227262. S2CID 3014674.
  2. ^ Hurst GD, Hurst LD, Johnstone RA (November 1992). "Intranuclear conflict and its role in evolution". Trends in Ecology & Evolution. 7 (11): 373–8. doi:10.1016/0169-5347(92)90007-x. PMID 21236071.
  3. ^ Hurst LD, Atlan A, Bengtsson BO (September 1996). "Genetic conflicts". The Quarterly Review of Biology. 71 (3): 317–64. doi:10.1086/419442. PMID 8828237. S2CID 24853836.
  4. ^ Hurst GD, Werren JH (August 2001). "The role of selfish genetic elements in eukaryotic evolution". Nature Reviews. Genetics. 2 (8): 597–606. doi:10.1038/35084545. PMID 11483984. S2CID 2715605.
  5. ^ McLaughlin RN, Malik HS (January 2017). "Genetic conflicts: the usual suspects and beyond". The Journal of Experimental Biology. 220 (Pt 1): 6–17. doi:10.1242/jeb.148148. PMC 5278622. PMID 28057823.
  6. ^ Gardner A, Úbeda F (December 2017). "The meaning of intragenomic conflict" (PDF). Nature Ecology & Evolution. 1 (12): 1807–1815. Bibcode:2017NatEE...1.1807G. doi:10.1038/s41559-017-0354-9. hdl:10023/13307. PMID 29109471. S2CID 3314539.
  7. ^ Williams GC (2008-09-02). Adaptation and Natural Selection A Critique of Some Current Evolutionary Thought. Princeton University Press. ISBN 978-1-4008-2010-8.
  8. ^ Dawkins R (1976). The Selfish Gene. Oxford University Press. ISBN 978-0-19-109306-7. OCLC 953456293.
  9. ^ Orgel LE, Crick FH (April 1980). "Selfish DNA: the ultimate parasite". Nature. 284 (5757): 604–7. Bibcode:1980Natur.284..604O. doi:10.1038/284604a0. PMID 7366731. S2CID 4233826.
  10. ^ Doolittle WF, Sapienza C (April 1980). "Selfish genes, the phenotype paradigm and genome evolution". Nature. 284 (5757): 601–3. Bibcode:1980Natur.284..601D. doi:10.1038/284601a0. PMID 6245369. S2CID 4311366.
  11. ^ Burt A, Trivers R (2006-01-31). Genes in Conflict. Cambridge, MA and London, England: Harvard University Press. doi:10.4159/9780674029118. ISBN 978-0-674-02911-8. S2CID 90469073.
  12. ^ Werren JH (June 2011). "Selfish genetic elements, genetic conflict, and evolutionary innovation". Proceedings of the National Academy of Sciences of the United States of America. 108 Suppl 2 (Supplement 2): 10863–70. Bibcode:2011PNAS..10810863W. doi:10.1073/pnas.1102343108. PMC 3131821. PMID 21690392.

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