Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

ACCESS DATA

Json Xml

Dataset's files

Source:

			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

Items per page:

1 - 5 of 19

Similar Datasets

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

| PRJNA288729 | ENA

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

Caenorhabditis virilis

Project description:Caenorhabditis virilis overview

| PRJNA1111183 | ENA

Drosophila virilis

Project description:Drosophila virilis Genome sequencing

| PRJNA242283 | ENA

Drosophila virilis

Project description:Drosophila virilis Raw sequence reads

| PRJNA413683 | ENA