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The hrde-1 mutation suppresses the rde-11 and sid-1 sRNA upregulation phenotype of meg-3 meg-4 mutants

ABSTRACT: The hrde-1 mutation suppresses the rde-11 and sid-1 sRNA upregulation phenotype of meg-3 meg-4 mutants

PROVIDER: PRJNA555889 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9725733.fastq.gz	Fastqsanger.gz
	SRR9725734.fastq.gz	Fastqsanger.gz
	SRR9725735.fastq.gz	Fastqsanger.gz
	SRR9725736.fastq.gz	Fastqsanger.gz
	SRR9725737.fastq.gz	Fastqsanger.gz

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The hrde-1 mutation suppresses the rde-11 and sid-1 sRNA upregulation phenotype of meg-3 meg-4 mutants

Project description:sRNAseq was conducted on the hrde-1; meg-3 meg-4 triple mutant, revealing that the hrde-1 mutation suppresses the rde-11 and sid-1 sRNA upregulation phenotype of meg-3 meg-4 mutants .

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meg-3 meg-4 upregulate endogenous sRNAs targeting RNAi genes and downregulate their mRNAs

Project description:sRNAseq was conducted on four independently generated meg-3 meg-4 lines, and upregulation of sRNAs targeting several RNAi genes was found. mRNAseq found that the transcript levels for several of these genes was also down. meg-3 meg-4 mutants also showed a similar pattern of sRNA misregulation as the rde-11 mutant.

2019-07-23 | GSE134628 | GEO

meg-3 meg-4 mutants are defective in exogenous RNAi signal amplification

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Germ granules coordinate RNA-based epigenetic inheritance pathways

Project description:Germ granules are biomolecular condensates that promote germ cell totipotency in most, if not all, animals. In C. elegans, MEG-3 and MEG-4 are two intrinsically disordered proteins that are redundantly required for the phase separations that drive germ granule assembly in germline blastomeres. Here, we show that animals lacking MEG-3/4 exhibit defects in dsRNA-mediated gene silencing (RNAi) that are due, at least in part, to defects in systemic RNAi. Interestingly, these RNAi defects are transgenerationally disconnected from meg-3/4 genotype: RNAi defects do not arise until 5-9 generations after animals become mutant for meg-3/4, and RNAi defects persist for 9-11 generations after meg-3/4 genotype is restored to wild type. Similar non-Mendelian patterns of inheritance are associated with other mutations that disrupt germ granule formation, indicating that germ granule disruption is the likely cause of genotype/phenotype disconnects. Loss of germ granules is associated with the production of aberrant populations of endogenous siRNAs, which, remarkably, are propagated for ≅10 generations in wild-type descendants of animals that lacked germ granules. sid-1, which encodes a factor required for systemic RNAi in C. elegans, is inappropriately and heritably silenced by aberrantly expressed sid-1 endogenous siRNAs, suggesting that transgenerational silencing of sid-1 likely underlies the heritable defect in RNAi. We conclude that one function of germ granules is to organize RNA-based epigenetic inheritance pathways and that failure to assemble germ granules has consequences that persist across many generations.

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The gene expression upon dominant negative form of GAS2 (GAS2DN) in MEG-01 cells

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Project description:Pseudoalteromonas sp. meg-B1 Genome sequencing and assembly

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