Epigenetic Regulation of A Heat-Activated Retrotransposon in Cruciferous Vegetables

Nozawa, Kohei; Kawagishi, Yuki; Kawabe, Akira; Sato, Mio; Masuta, Yukari; Kato, Atsushi; Ito, Hidetaka

doi:10.20944/preprints201705.0022.v1

Cited by 1 publication

(1 citation statement)

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“…The increased rates of TE activity allow populations to explore the fitness landscape. The epi-transposon hypothesis has been explored more completely in plant studies (for examples see Ito et al 2016 ; Nozawa et al 2017 ) than in vertebrates. Despite these limitations general observations in the human genome, including increases in TE expression due to chemical exposure, approximating environmental stress (Kale et al 2005 ), and the association of TEs in stress related gene regions (van de Lagemaat et al 2003 ), tend to support tenets of the epi-transposons hypothesis.…”

Section: Impacts Of Advantageous Te Insertions On Mammalian Genomesmentioning

confidence: 99%

Mammalian transposable elements and their impacts on genome evolution

2018

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Transposable elements (TEs) are genetic elements with the ability to mobilize and replicate themselves in a genome. Mammalian genomes are dominated by TEs, which can reach copy numbers in the hundreds of thousands. As a result, TEs have had significant impacts on mammalian evolution. Here we summarize the current understanding of TE content in mammal genomes and find that, with a few exceptions, most fall within a predictable range of observations. First, one third to one half of the genome is derived from TEs. Second, most mammalian genomes are dominated by LINE and SINE retrotransposons, more limited LTR retrotransposons, and minimal DNA transposon accumulation. Third, most mammal genome contains at least one family of actively accumulating retrotransposon. Finally, horizontal transfer of TEs among lineages is rare. TE exaptation events are being recognized with increasing frequency. Despite these beneficial aspects of TE content and activity, the majority of TE insertions are neutral or deleterious. To limit the deleterious effects of TE proliferation, the genome has evolved several defense mechanisms that act at the epigenetic, transcriptional, and post-transcriptional levels. The interaction between TEs and these defense mechanisms has led to an evolutionary arms race where TEs are suppressed, evolve to escape suppression, then are suppressed again as the defense mechanisms undergo compensatory change. The result is complex and constantly evolving interactions between TEs and host genomes.

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