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Stochastic gain of susceptibility suggests a novel mechanism of resistance to hybrid dysgenesis in Drosophila virilis

ABSTRACT: Stochastic gain of susceptibility suggests a novel mechanism of resistance to hybrid dysgenesis in Drosophila virilis

PROVIDER: PRJNA423051 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6391750.fastq.gz	Fastqsanger.gz
	SRR6391760.fastq.gz	Fastqsanger.gz
	SRR6391751.fastq.gz	Fastqsanger.gz
	SRR6391761.fastq.gz	Fastqsanger.gz
	SRR6391752.fastq.gz	Fastqsanger.gz

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Stochastic gain of susceptibility suggests a novel mechanism of resistance to hybrid dysgenesis in Drosophila virilis

Project description:Syndromes of hybrid dysgenesis (HD) have been critical for our understanding of the transgenerational maintenance of genome stability by piRNA. HD in D. virilis represents a special case of HD since it includes simultaneous mobilization of a set of TEs that belong to different classes. The standard explanation for HD is that eggs of the responder strains lack an abundant pool of piRNAs corresponding to the asymmetric TE families transmitted solely by sperm. However, there are several strains of D. virilis that lack asymmetric TEs, but exhibit a “neutral” cytotype that confers resistance to HD. To characterize the mechanism of resistance to HD, we performed a comparative analysis of the landscape of ovarian small RNAs in strains that vary in their resistance to HD mediated sterility. We demonstrate that resistance to HD cannot be solely explained by a maternal piRNA pool that matches the assemblage of TEs that likely cause HD. In support of this, we have witnessed a cytotype shift from neutral (N) to susceptible (M) in a strain devoid of all major TEs implicated in HD. This shift occurred in the absence of significant change in TE copy number and expression of piRNAs homologous to asymmetric TEs. Instead, this shift is associated with a change in the chromatin profile of repeat sequences unlikely to be causative of paternal induction. Overall, our data suggest that resistance to TE-mediated sterility during HD may be achieved by mechanisms that are distinct from the canonical syndromes of HD.

2017-12-20 | GSE108298 | GEO

Drosophila virilis

Project description:Analysis of Hybrid Dysgenesis in Drosophila virilis

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Spontaneous gain of susceptibility suggests a novel mechanism of resistance to hybrid dysgenesis in Drosophila virilis.

Project description:Syndromes of hybrid dysgenesis (HD) have been critical for our understanding of the transgenerational maintenance of genome stability by piRNA. HD in D. virilis represents a special case of HD since it includes simultaneous mobilization of a set of TEs that belong to different classes. The standard explanation for HD is that eggs of the responder strains lack an abundant pool of piRNAs corresponding to the asymmetric TE families transmitted solely by sperm. However, there are several strains of D. virilis that lack asymmetric TEs, but exhibit a "neutral" cytotype that confers resistance to HD. To characterize the mechanism of resistance to HD, we performed a comparative analysis of the landscape of ovarian small RNAs in strains that vary in their resistance to HD mediated sterility. We demonstrate that resistance to HD cannot be solely explained by a maternal piRNA pool that matches the assemblage of TEs that likely cause HD. In support of this, we have witnessed a cytotype shift from neutral (N) to susceptible (M) in a strain devoid of all major TEs implicated in HD. This shift occurred in the absence of significant change in TE copy number and expression of piRNAs homologous to asymmetric TEs. Instead, this shift is associated with a change in the chromatin profile of repeat sequences unlikely to be causative of paternal induction. Overall, our data suggest that resistance to TE-mediated sterility during HD may be achieved by mechanisms that are distinct from the canonical syndromes of HD.

| S-EPMC5993320 | biostudies-literature

RNA profiling in Drosophila virilis and Drosophila yakuba

Project description:Gene annoation and determination of gene expression levels in Drosophila virilis and Drosophila yakuba by deep sequencing.

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Project description:Drosophila virilis Genome sequencing

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Small RNA expression throughout the development of Drosophila virilis

Project description:Examination of temporal small RNA expression during the embryonic development, larval and adult stages of Drosophila virilis

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Project description:Drosophila virilis Raw sequence reads

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RNA profiling in Drosophila virilis and Drosophila yakuba

Project description:Gene annoation and determination of gene expression levels in Drosophila virilis and Drosophila yakuba by deep sequencing. Total RNA-seq data from heads of 2-5 day old mated D virilis and D yakuba females, 1 sample from each species.

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Time course Chromatin Immunoprecipitation on Drosophila virilis embryos during embryogenesis

Project description:ChIP followed by next generation sequencing over 5 developmental time points of Drosophila virilis embryos (w[-], white eye mutation line) against 5 key mesodermal factors (Twist, Tinman, Mef2, Bagpipe and Biniou) were performed. The aim was to compare binding profiles of these 5 mesodermal factors between two Drosophila species, D. melanogaster (Zinzen et al., 2009) and D. virilis (this study). D. virilis specific antibodies were used for this purpose for 4 of the 5 factors (D. melanogaster Anti-body for Mef2 showed high specificity in D. virilis). Two biological replicates for each condition were sequenced using Illumina HiSeq.

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Project description:Drosophila virilis Transcriptome or Gene expression

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