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Series GSE103582 Query DataSets for GSE103582
Status Public on Dec 06, 2017
Title piRNA-mediated regulation of transposon alternative splicing in soma and germline
Organism Drosophila melanogaster
Experiment type Genome binding/occupancy profiling by high throughput sequencing
Expression profiling by high throughput sequencing
Summary Transposable elements can drive genome evolution, but their enhanced activity is detrimental to the host and therefore must be tightly regulated. The piwi-interacting small RNAs (piRNAs) pathway is critically important for transposable element regulation, by inducing transcriptional silencing or post-transcriptional decay of mRNAs. We show that piRNAs and piRNA biogenesis components regulate pre-mRNA splicing of P transposable element transcripts in vivo, leading to the production of the non-transposase-encoding mature mRNA isoform in germ cells. Unexpectedly, we show that the piRNA pathway components do not act to reduce P-element transposon transcript levels during P-M hybrid dysgenesis, a syndrome that affects germline development in Drosophila. Instead, splicing regulation is mechanistically achieved in concert with piRNA-mediated changes to repressive chromatin states, and relies on the function of the Piwi-piRNA complex proteins Asterix/Gtsf1 and Panoramix/Silencio, as well as Heterochromatin Protein 1a (Su(var)205/HP1a). Furthermore, we show that this machinery, together with the piRNA Flamenco cluster, not only controls the accumulation of Gypsy retrotransposon transcripts but also regulates splicing of Gypsy mRNAs in cultured ovarian somatic cells, a process required for the production of infectious particles that can lead to heritable transposition events. Our findings identify splicing regulation as a new role and essential function for the Piwi pathway in protecting the genome against transposon mobility, and provide a model system for studying the role of chromatin structure in modulating alternative splicing during development.
 
Overall design ChIP-seq: two samples (non-dysgenic and dysgenic F1 progeny) were analyzed in biological replicates. RNA-seq: three comparisons [non-dysgenic vs. dysgenic F1 progeny; aub heterozygous vs. aub mutant (in Harwich background); and piwi heterozygous vs. piwi mutant (in Harwich background)] were analyzed in biological replicates.
 
Contributor(s) Teixeira FK, Okuniewska M, Malone CD, Coux R, Rio DC, Lehmann R
Citation(s) 29211718
NIH grant(s)
Grant ID Grant title Affiliation Name
R37 HD041900 Germ Cell Migration in Drosophila. NEW YORK UNIVERSITY SCHOOL OF MEDICINE RUTH LEHMANN
R01 GM097352 Alternative pre-mRNA Splicing in Drosophila UNIVERSITY OF CALIFORNIA BERKELEY DONALD C RIO
R35 GM118121 DNA transposons and alternative pre-mRNA splicing UNIVERSITY OF CALIFORNIA BERKELEY DONALD C RIO
Submission date Sep 07, 2017
Last update date Jul 25, 2021
Contact name Felipe Karam Teixeira
E-mail(s) Felipe.Teixeira@med.nyu.edu
Organization name New York University Medical Center
Department Skirball Institute
Street address 540 1st Avenue
City New York
State/province New York
ZIP/Postal code 10016
Country USA
 
Platforms (1)
GPL17275 Illumina HiSeq 2500 (Drosophila melanogaster)
Samples (20)
GSM2774790 ChIPseq_input_non_dysgenic_rep1
GSM2774791 ChIPseq_input_non_dysgenic_rep2
GSM2774792 ChIPseq_input_dysgenic_rep1
Relations
BioProject PRJNA401989
SRA SRP117017

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Supplementary file Size Download File type/resource
GSE103582_RAW.tar 2.2 Gb (http)(custom) TAR (of BEDGRAPH, BIGWIG)
SRA Run SelectorHelp
Raw data are available in SRA
Processed data provided as supplementary file

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