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

ABSTRACT: 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.

ORGANISM(S): Caenorhabditis elegans

PROVIDER: GSE134627 | GEO | 2019/07/23

REPOSITORIES: GEO

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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

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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.

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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.

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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.

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Specialized germline P-bodies are required to specify germ cell fate 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 describe 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.

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

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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.

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