Dataset features
Specifications
Application: | RNA-seq analysis |
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Number of samples: | 5 |
Release date: | Jan 1 2017 |
Last update date: | May 2 2018 |
Access: | Public |
Diseases: | Neoplasms, Second Primary |
Computational protocol: | Bowtie, D3.js |
Dataset link | Decoupling the downstream effects of germline nuclear RNAi reveals that transcriptional repression and heritable RNAi are independent of the H3K9me3 response in C. elegans [pre-mRNA-seq] |
Experimental Protocol
In this study we tested if RNAi-mediated H3K9me3 is required for the heritable RNAi and transcriptional silencing at native endogenous and exogenous RNAi targets. Using genetic approach we generated nearly completely deficient H3K9me3 worm strain (met-2;set-25;set-32). Using Pol II ChIP-seq, pre-mRNA-seq and mRNA-seq we validated transcriptional changes at the endogenous targets in the H3K9me3 deficient condition (met-2;set-25;set-32). We performed oma-1 dsRNA feeding and heritable RNAi experiment and using H3K9me3 ChIP-seq measured level of RNAi-triggered H3K9me3 contribution by set-32 or met-2;set-25 or met-2;set-25;set-32 HMTs at the oma-1 gene. Using oma-1 mRNA and pre-mRNA qRT-PCR we tested heritable RNAi effect at oma-1 genomic locus in these HMT mutants.
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Sam Gu
Dataset Statistics
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Citations per year
Dataset publication
2017
Epigenetics Chromatin
PMCID: 5311726
PMID: 28228846
DOI: 10.1186/s13072-017-0114-8
call_split See protocol