@article{fdi:010074521,
  title = {{T}he somatic pi{RNA} pathway controls germline transposition over generations},
  author = {{B}arckmann, {B}. and {E}l-{B}arouk, {M}. and {P}elisson, {A}. and {M}ugat, {B}. and {L}i, {B}. and {F}ranckhauser, {C}. and {L}avier, {A}. {S}. {F}. and {M}irouze, {M}arie and {F}ablet, {M}. and {C}hambeyron, {S}.},
  editor = {},
  language = {{ENG}},
  abstract = {{T}ransposable elements ({TE}s) are parasitic {DNA} sequences that threaten genome integrity by replicative transposition in host gonads. {T}he {P}iwi-interacting {RNA}s (pi{RNA}s) pathway is assumed to maintain {D}rosophila genome homeostasis by downregulating transcriptional and post-transcriptional {TE} expression in the ovary. {H}owever, the bursts of transposition that are expected to follow transposome derepression after pi{RNA} pathway impairment have not yet been reported. {H}ere, we show, at a genome-wide level, that pi{RNA} loss in the ovarian somatic cells boosts several families of the endogenous retroviral subclass of {TE}s, at various steps of their replication cycle, from somatic transcription to germinal genome invasion. {F}or some of these {TE}s, the derepression caused by the loss of pi{RNA}s is backed up by another small {RNA} pathway (si{RNA}s) operating in somatic tissues at the post transcriptional level. {D}erepressed transposition during 70 successive generations of pi{RNA} loss exponentially increases the genomic copy number by up to 10-fold.},
  keywords = {},
  booktitle = {},
  journal = {{N}ucleic {A}cids {R}esearch},
  volume = {46},
  numero = {18},
  pages = {9524--9536},
  ISSN = {0305-1048},
  year = {2018},
  DOI = {10.1093/nar/gky761},
  URL = {https://www.documentation.ird.fr/hor/fdi:010074521},
}