Project description:Transposable elements (TEs) are genomic parasite that threat genome integrity. One major strategy organisms evolved to balance TE activity in the germline is the Piwi-interacting RNAs (piRNAs) pathway. It prevents transposition by repressing TE at transcriptional and/or post-transcriptional level. However, evidence that TE derepression caused by piRNA pathway impairment is actually followed by bursts of transposition is still lacking. Here we present a genome-wide TE-analyses of the replicative TE life cycle (their expression, their translation to their transposition in the germline) after piRNA pathway impairment in the somatic follicle cells. We observed a high transposition-rate in the germline, leading to a 10-fold increase in genomic TE-load after 70 successive generations of piRNA pathway impairment. Moreover, we demonstrate that siRNAs co-regulate TE activity at post transcriptional level in follicle cells. These observations demonstrate that the small RNA-mediated TE repression in follicle cells contribute to genome homeostasis.
Project description:Transposable elements (TEs) are genomic parasite that threat genome integrity. One major strategy organisms evolved to balance TE activity in the germline is the Piwi-interacting RNAs (piRNAs) pathway. It prevents transposition by repressing TE at transcriptional and/or post-transcriptional level. However, evidence that TE derepression caused by piRNA pathway impairment is actually followed by bursts of transposition is still lacking. Here we present a genome-wide TE-analyses of the replicative TE life cycle (their expression, their translation to their transposition in the germline) after piRNA pathway impairment in the somatic follicle cells. We observed a high transposition-rate in the germline, leading to a 10-fold increase in genomic TE-load after 70 successive generations of piRNA pathway impairment. Moreover, we demonstrate that siRNAs co-regulate TE activity at post transcriptional level in follicle cells. These observations demonstrate that the small RNA-mediated TE repression in follicle cells contribute to genome homeostasis.
Project description:Transposable elements (TEs) are genomic parasite that threat genome integrity. One major strategy organisms evolved to balance TE activity in the germline is the Piwi-interacting RNAs (piRNAs) pathway. It prevents transposition by repressing TE at transcriptional and/or post-transcriptional level. However, evidence that TE derepression caused by piRNA pathway impairment is actually followed by bursts of transposition is still lacking. Here we present a genome-wide TE-analyses of the replicative TE life cycle (their expression, their translation to their transposition in the germline) after piRNA pathway impairment in the somatic follicle cells. We observed a high transposition-rate in the germline, leading to a 10-fold increase in genomic TE-load after 70 successive generations of piRNA pathway impairment. Moreover, we demonstrate that siRNAs co-regulate TE activity at post transcriptional level in follicle cells. These observations demonstrate that the small RNA-mediated TE repression in follicle cells contribute to genome homeostasis.
Project description:Transposable elements (TEs) are genomic parasite that threat genome integrity. One major strategy organisms evolved to balance TE activity in the germline is the Piwi-interacting RNAs (piRNAs) pathway. It prevents transposition by repressing TE at transcriptional and/or post-transcriptional level. However, evidence that TE derepression caused by piRNA pathway impairment is actually followed by bursts of transposition is still lacking. Here we present a genome-wide TE-analyses of the replicative TE life cycle (their expression, their translation to their transposition in the germline) after piRNA pathway impairment in the somatic follicle cells. We observed a high transposition-rate in the germline, leading to a 10-fold increase in genomic TE-load after 70 successive generations of piRNA pathway impairment. Moreover, we demonstrate that siRNAs co-regulate TE activity at post transcriptional level in follicle cells. These observations demonstrate that the small RNA-mediated TE repression in follicle cells contribute to genome homeostasis.
Project description:Transposable elements (TEs) are parasitic DNA sequences that threaten genome integrity by replicative transposition in host gonads. The Piwi-interacting RNAs (piRNAs) pathway is assumed to maintain Drosophila genome homeostasis by downregulating transcriptional and post-transcriptional TE expression in the ovary. However, the bursts of transposition that are expected to follow transposome derepression after piRNA pathway impairment have not yet been reported. Here, we show, at a genome-wide level, that piRNA loss in the ovarian somatic cells boosts several families of the endogenous retroviral subclass of TEs, at various steps of their replication cycle, from somatic transcription to germinal genome invasion. For some of these TEs, the derepression caused by the loss of piRNAs is backed up by another small RNA pathway (siRNAs) operating in somatic tissues at the post transcriptional level. Derepressed transposition during 70 successive generations of piRNA loss exponentially increases the genomic copy number by up to 10-fold.