Abstract
Transposons are infectious agents in sexual populations and can go to fixation even if they reduce the fitness of the host. Sexual hosts are therefore under selective pressure to evolve defensive functions that relieve the fitness penalty imposed by transposons. In mammals, this defensive function depends on transcriptional silencing through targeted cytosine methylation of transposon promoters in both germ-line and somatic tissues (with the probable involvement of some post-transcriptional gene silencing by pathways related to RNA interference). New families of transposons evolve in response to selective pressures imposed by host silencing mechanisms, with the result that the mammalian genome has suffered waves of transposon bombardment that have contributed the majority of the total sequence. Cytosine methylation defends the sexual genome against transposon damage even as it enforces a requirement for sexual reproduction through the phenomenon of genomic imprinting.
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