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Transcriptional analysis of early and late generation nuclear RNAi deficient animals

ABSTRACT: Transcriptional analysis of early and late generation nuclear RNAi deficient animals

PROVIDER: PRJNA478309 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7446950.fastq.gz	Fastqsanger.gz
	SRR7446960.fastq.gz	Fastqsanger.gz
	SRR7446951.fastq.gz	Fastqsanger.gz
	SRR7446961.fastq.gz	Fastqsanger.gz
	SRR7446952.fastq.gz	Fastqsanger.gz

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Transcriptional analysis of early and late generation nuclear RNAi deficient animals

Project description:Transcriptional analysis of early and late generation nuclear RNAi deficient animals

| PRJNA478309 | ENA

Transcriptional analysis of early and late generation nuclear RNAi deficient animals

Project description:Germ cells deficient for Piwi and associated small RNA genome silencing factors transmit a form of heritable stress that induces sterility after growth for several generations. The cause of this transgenerational sterility phenotype is not understood but has been attributed to progressive deterioration of heterochromatin and associated DNA damage. Sterile small RNA genome silencing mutants displayed inconsistent increases in DNA damage signaling but consistently altered perinuclear germ granules. Germ granule dysfunction was sufficient to induce phenotypes associated with sterile small RNA genome silencing mutants, including germline atrophy, reproductive diapause and univalents in oocytes. Genes that perturb germ granule structure were not compromised in sterile small RNA mutants, suggesting a post-transcriptional reproductive arrest mechanism. We conclude that the integrity of germ granules, which are intimately associated with Piwi silencing factors, orchestrates the sterility of Piwi deficient mutants and could be generally relevant to regulation of reproductive arrest in response to stress.

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Gene expression profiles of Six1/2-1(RNAi) animals and POU2/3(RNAi) animals

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Gene expression profiles of Fir1 (RNAi) animals

Project description:The goal of this study was to identify Fir1 downstream genes that were required for local proliferation. Fir1(RNAi) animals displayed reduced local proliferation near the wound,while the proliferation far from the wound was not decreased after Fir1 RNAi. The regenerating pieces following Fir1 RNAi were expected to only show decreased levels of the genes near the wound relative to control RNAi animals.

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Retinal transcriptomes of Plk3-deficient animals

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Gene expression profiles of Six1/2-1(RNAi) animals and POU2/3(RNAi) animals

Project description:The goal of this study was to identify genes that were expressed in the protonephridial system. Because Six1/2(RNAi) and POU2/3(RNAi) animals lose the tubules, flame cells and accessory cells, these animals were expected to show decreased levels of the genes expressed in the nephridial system relative to control RNAi animals. RNA from Six1/2(RNAi) and POU2/3(RNAi) animals was harvested with Trizol at days 8 and 15 after RNAi initiation for the former and days 15 and 21 for the latter. Three biological replicates were used. RNA from the four samples were competetively hybridized on a microarray with RNA from control RNAi animals of the corresponding days.

2011-11-28 | E-GEOD-31618 | biostudies-arrayexpress

Retinal transcriptome analysis of Rbfox2 deficient animals

Project description:Retinal transcriptome analysis of Rbfox2 deficient animals

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mRNA expression analysis in mock and cgh-1(RNAi) animals

Project description:To determine mRNA expression levels in mock and cgh-1(RNAi) animals, RNA was purified from young adult worms, using Trizol.

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RNA-seq from L4 animals treated with RNAi against gfp (control), ham-3, and swsn-2.2

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morc-1 regulates transgenerational heterochromatin maintenance at nuclear RNAi targets

Project description:The germline is an immortal cell lineage and therefore must accurately transmit genetic and epigenetic information over infinite cell divisions to ensure fertility and species survival. Endogenous siRNAs (endo-siRNAs), which are highly expressed in the parental germline and inherited in their progeny, represent one mechanism by which epigenetic information can be transmitted from one generation to the next. In C. elegans, this is accomplished by the nuclear RNAi pathway, which ensures robust inheritance of endo-siRNAs and of target gene silencing through deposition of H3K9me3 marks at target loci. How these marks are maintained in subsequent generations is unknown. Here, we show that the C. elegans micro-orchidia homolog, MORC-1, functions downstream of endo-siRNAs to mediate target silencing and maintenance of siRNA-dependent H3K9me3 marks. Like the established members of the nuclear RNAi pathway, morc-1 is essential for germline maintenance and thus morc-1(-) mutants exhibit a mortal germline phenotype. Furthermore, morc-1(-) mutants exhibit severe decondensation of germline chromatin. Through a forward genetic screen, we have identified mutations in the gene encoding MET-1, a H3K36 histone methyltransferase, that potently suppress morc-1(-) germline mortality. We show that morc-1(-) mutants exhibit progressive, met-1-dependent enrichment of H3K36me3 and that mutation of met-1 can restore germline chromatin organization in late generation morc-1(-) mutants. Our data suggest that MORC-1 is required to repress MET-1 activity at nuclear RNAi target genes and that in the absence of this repression, MET-1-mediated encroachment of euchromatin leads to detrimental decondensation of germline chromatin and germline mortality.

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