| Literature DB >> 30057117 |
Lu Wang1, Kun Dou1, Sungjin Moon1, Frederick J Tan1, Zz Zhao Zhang2.
Abstract
Although animals have evolved multiple mechanisms to suppress transposons, "leaky" mobilizations that cause mutations and diseases still occur. This suggests that transposons employ specific tactics to accomplish robust propagation. By directly tracking mobilization, we show that, during a short and specific time window of oogenesis, retrotransposons achieve massive amplification via a cell-type-specific targeting strategy. Retrotransposons rarely mobilize in undifferentiated germline stem cells. However, as oogenesis proceeds, they utilize supporting nurse cells-which are highly polyploid and eventually undergo apoptosis-as factories to massively manufacture invading products. Moreover, retrotransposons rarely integrate into nurse cells themselves but, instead, via microtubule-mediated transport, they preferentially target the DNA of the interconnected oocytes. Blocking microtubule-dependent intercellular transport from nurse cells significantly alleviates damage to the oocyte genome. Our data reveal that parasitic genomic elements can efficiently hijack a host developmental process to propagate robustly, thereby driving evolutionary change and causing disease.Entities:
Keywords: germ cell; oogenesis; piRNA; transposon
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Year: 2018 PMID: 30057117 PMCID: PMC6628338 DOI: 10.1016/j.cell.2018.06.040
Source DB: PubMed Journal: Cell ISSN: 0092-8674 Impact factor: 41.582