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Caenorhabditis elegans

ABSTRACT: Post-transcriptional regulation by the let-7 microRNA and the TRIM-NHL protein LIN41 [Ribosome footprinting]

PROVIDER: PRJNA318047 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR3356480.fastq.gz	Fastqsanger.gz
	SRR3356490.fastq.gz	Fastqsanger.gz
	SRR3356500.fastq.gz	Fastqsanger.gz
	SRR3356510.fastq.gz	Fastqsanger.gz
	SRR3356520.fastq.gz	Fastqsanger.gz

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Caenorhabditis elegans

Project description:Post-transcriptional regulation by the let-7 microRNA and the TRIM-NHL protein LIN41 [RNA-seq]

| PRJNA318054 | ENA

Post-transcriptional regulation by the let-7 microRNA and the TRIM-NHL protein LIN41

Project description:Post-transcriptional regulation by the let-7 microRNA and the TRIM-NHL protein LIN41

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Project description:Extensive oscillatory gene expression during C. elegans larval development [Ribosome footprinting]

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Simultaneous activation of Tor and suppression of ribosome biogenesis by TRIM-NHL proteins promotes terminal differentiation

Project description:Tissue development and homeostasis depend on the balance between growth and terminal differentiation, but the mechanisms coordinating these processes remain elusive. Accumulating evidence indicates that ribosome biogenesis (RiBi) and protein synthesis, two cellular processes sustaining growth, are tightly regulated and yet can be uncoupled during stem cell differentiation. Using the Drosophila adult female germline stem cell (GSC) and larval neuroblast (NB) systems, we show that Mei-P26 and Brat, two Drosophila TRIM-NHL paralogs, are responsible for uncoupling RiBi and protein synthesis during differentiation. In differentiating cells, Mei-P26 and Brat activate the Target of rapamycin (Tor) kinase to promote translation, while concomitantly repressing RiBi. Depletion of Mei-P26 or Brat results in defective terminal differentiation, which can be rescued by ectopic activation of Tor together with suppression of RiBi. Our results indicate that uncoupling RiBi and translation activities by TRIM-NHL activity creates the conditions required for terminal differentiation.

2023-03-03 | GSE218205 | GEO

RNA co-immunoprecipitation coupled to RNA sequencing (RIP-seq) to identify somatic target mRNAs of the TRIM-NHL protein LIN41

Project description:RNA co-immunoprecipitation coupled to RNA sequencing (RIP-seq) to identify somatic target mRNAs of the TRIM-NHL protein LIN41

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Caenorhabditis elegans strain:N2

Project description:Caenorhabditis elegans Raw sequence reads NHL-2

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Identification of Meiotic-P26-bound RNAs in cutlured Drosophila SL2 cells by iCLIP (individual-nucleotide resolution UV crosslinking and immunoprecipitation)

Project description:The TRIM-NHL protein Meiotic P26 (Mei-P26) governs gene expression and controls stem cell fate in Drosophila. Mei-P26 represses the translation of the key regulator protein Nanos and induces miRNA-dependent silencing to regulate stem cell renewal, differentiation and proliferation. The structural and mechanistic details of mRNA target recognition and RNA binding by its C-terminal NHL domain remain elusive. To identify its cellular target RNAs, we performed iCLIP2 experiments in cultured Drosophila SL2 cells that were transfected with Flag-tagged Mei-P26 full-length, or its NHL domain.

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Project description:Transcriptome-wide measurement of ribosomal occupancy by ribosome profiling

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A microRNA family exerts maternal control on sex determination in C. elegans

Project description:Gene expression in early animal embryogenesis is in large part controlled post-transcriptionally. Maternally-contributed microRNAs may therefore play important roles in early development. We have elucidated a major biological role of the nematode mir-35 family of maternally-contributed, essential microRNAs. We show that this microRNA family regulates the sex determination pathway at multiple levels, acting both upstream and downstream of her-1 to prevent aberrantly activated male developmental programs in hermaphrodite embryos. The predicted target genes that act downstream of the mir-35 family in this process, sup-26 and nhl-2, both encode RNA binding proteins, thus delineating a previously unknown post-transcriptional regulatory subnetwork within the well-studied sex determination pathway of C. elegans. Repression of nhl-2 by the mir-35 family is not only required for proper sex determination but also for viability, showing that a single microRNA target site can be essential. Since sex determination in C. elegans requires zygotic gene expression to read the sex chromosome karyotype, early embryos must remain gender-naïve; our findings show that the mir-35 family microRNAs act in the early embryo to function as a developmental timer that preserves naïveté and prevents premature deleterious developmental decisions. This SuperSeries is composed of the SubSeries listed below.

2017-02-09 | GSE94704 | GEO

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