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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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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 .

2019-07-23 | GSE134629 | GEO

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

Project description:Worms were fed a dsRNA trigger against the pos-1 gene and subjected to sRNAseq to see if they could amplify the exogenous RNAi trigger. meg-3 meg-4 were not able to amplify the signal as robustly as wild-type.

2019-07-23 | GSE134627 | GEO

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.

2019-08-08 | GSE134683 | GEO

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

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

| PRJNA555887 | ENA

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

2013-07-25 | GSE49184 | GEO

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

Project description:GAS2DN could suppress the growth of chronic myeloid leukemia cells, including K562, MEG-01 and CD34+ cells from patients. In addition, GAS2DN inhibited the tumorigenic ability of MEG-01 cells in nude mice. To understand the molecular insight of this inhibitory effect of GAS2DN, global gene expression were performed. The control and GAS2DN-transduced MEG-01 cells were used for microarray analysis. Three biological independent extracts of control and GAS2DN-transduced cells were pooled together with equal amount, and then the pooled samples were compared with Affymetrix chips.

2013-07-25 | E-GEOD-49184 | biostudies-arrayexpress

Pisolithus albus strain:Meg 11

Project description:Pisolithus albus Meg 11 Resequencing

| PRJNA444312 | ENA

Protein-protein interactions of MEG-3 in C. elegans early embryos

Project description:We combined in vivo expressed GFP-tagged MEG-3 (GEI-12) with label-free quantitative proteomics to identify protein-protein interactions of MEG-3 in early C. elegans embryos.

2021-07-01 | PXD012852 | Pride

Protein interactors of MEG-1 in C. elegans embryos

Project description:In animals with germ plasm, specification of the germline involves “germ granules”, cytoplasmic condensates that enrich maternal transcripts in the germline founder cells. In C. elegans embryos, P granules enrich maternal transcripts, but surprisingly P granules are not essential for germ cell fate specification. Here we have described a second condensate in the C. elegans germ plasm. Like canonical P-bodies found in somatic cells, “germline P-bodies” contain regulators of mRNA decapping and deadenylation and, in addition, the intrinsically-disordered proteins MEG-1 and MEG-2 and the TIS11-family RNA-binding protein POS-1. Embryos lacking meg-1 and meg-2 do not stabilize P-body components, miss-regulate POS-1 targets, miss-specify the germline founder cell, and do not develop a germline. Our findings suggest that specification of the germ line involves at least two distinct condensates that independently enrich and regulate maternal mRNAs in the germline founder cells.

2022-10-05 | PXD036610 | Pride

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