Caenorhabditis elegans
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA251425 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR1314160.fastq.gz | Fastqsanger.gz | |||
| SRR1314161.fastq.gz | Fastqsanger.gz | |||
| SRR1314162.fastq.gz | Fastqsanger.gz | |||
| SRR1314156.fastq.gz | Fastqsanger.gz | |||
| SRR1314157.fastq.gz | Fastqsanger.gz |
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Project description:The double-stranded RNA-binding protein Staufen has been implicated in various posttranscriptional gene regulatory processes. Here, we demonstrate that the Caenorhabditis elegans homolog of Staufen, STAU-1, functionally interacts with microRNAs. Loss-of-function mutations of stau-1 significantly suppress phenotypes of let-7 family microRNA mutants, a hypomorphic allele of dicer and a lsy-6 microRNA partial loss-of-function mutant. Furthermore, STAU-1 modulates the activity of lin-14, a target of lin-4 and let-7 family microRNAs, and this modulation is abolished when the 3' untranslated region of lin-14 is removed. Deep sequencing of small RNA cDNA libraries reveals no dramatic change in the levels of microRNAs, or other small RNA populations between wild-type and stau-1 mutants, with the exception of certain endogenous siRNAs in the WAGO pathway. The modulation of microRNA activity by STAU-1 does not seem to be associated with the previously reported enhanced exogenous RNAi (Eri) phenotype of stau-1 mutants, since eri-1 exhibits the opposite effect on microRNA activity. Altogether, our results suggest that STAU-1 negatively modulates microRNA activity downstream of biogenesis, possibly by competing with microRNAs for binding on the 3' untranslated region of target mRNAs
2016-03-16 | GSE79217 | GEO
Project description:Staufen Negatively Modulates MicroRNA Activity in Caenorhabditis elegans
| PRJNA315193 | ENA
Project description:The double-stranded RNA-binding protein Staufen has been implicated in various posttranscriptional gene regulatory processes. Here, we demonstrate that the Caenorhabditis elegans homolog of Staufen, STAU-1, functionally interacts with microRNAs. Loss-of-function mutations of stau-1 significantly suppress phenotypes of let-7 family microRNA mutants, a hypomorphic allele of dicer and a lsy-6 microRNA partial loss-of-function mutant. Furthermore, STAU-1 modulates the activity of lin-14, a target of lin-4 and let-7 family microRNAs, and this modulation is abolished when the 3' untranslated region of lin-14 is removed. Deep sequencing of small RNA cDNA libraries reveals no dramatic change in the levels of microRNAs, or other small RNA populations between wild-type and stau-1 mutants, with the exception of certain endogenous siRNAs in the WAGO pathway. The modulation of microRNA activity by STAU-1 does not seem to be associated with the previously reported enhanced exogenous RNAi (Eri) phenotype of stau-1 mutants, since eri-1 exhibits the opposite effect on microRNA activity. Altogether, our results suggest that STAU-1 negatively modulates microRNA activity downstream of biogenesis, possibly by competing with microRNAs for binding on the 3' untranslated region of target mRNAs Deep-sequencing was performed on cDNA libraries made from total RNA from young adults populations of two strains: wild-type (N2) and stau-1(tm2266), in three biological replicates each strain.
2016-03-16 | E-GEOD-79217 | biostudies-arrayexpress
Project description:The mammalian PAS-domain protein PERIOD (PER) and its C. elegans orthologue LIN-42 have been proposed to constitute an evolutionary link between two distinct, circadian and developmental, timing systems. However, while the function of PER in animal circadian rhythms is well understood molecularly and mechanistically, this is not true for LIN-42’s function in timing rhythmic development. Here, using targeted deletions, we find that the LIN-42 PAS domains are dispensable for the protein’s function in timing molts. Instead, we observe arrhythmic molts upon deletion of a distinct sequence element, conserved with PER. We show that this element, designated CK1δ-binding domain (CK1BD), mediates stable binding to KIN-20, the C. elegans CK1δ/ε orthologue. We demonstrate that CK1δ phosphorylates LIN-42 and define two conserved helical motifs in the CK1BD, CK1BD-A and CK1BD-B, that have distinct roles in controlling CK1δ-binding and kinase activity in vitro. KIN-20 and the LIN-42 CK1BD are required for proper molting timing in vivo, and loss of LIN-42 binding changes KIN-20 subcellular localization. The interactions mirror the central role of a stable circadian PER–CK1 complex in setting a robust ~24-hour period. Hence, our results establish LIN-42/PER – KIN-20/CK1δ/ε as a functionally conserved signaling module of two distinct chronobiological systems.
2025-10-10 | PXD058601 | Pride
Project description:The mammalian PAS-domain protein PERIOD (PER) and its C. elegans orthologue LIN-42 have been proposed to constitute an evolutionary link between two distinct, circadian and developmental, timing systems. However, while the function of PER in animal circadian rhythms is well understood molecularly and mechanistically, this is not true for LIN-42’s function in timing rhythmic development. Here, using targeted deletions, we find that the LIN-42 PAS domains are dispensable for the protein’s function in timing molts. Instead, we observe arrhythmic molts upon deletion of a distinct sequence element, conserved with PER. We show that this element, designated CK1δ-binding domain (CK1BD), mediates stable binding to KIN-20, the C. elegans CK1δ/ε orthologue. We demonstrate that CK1δ phosphorylates LIN-42 and define two conserved helical motifs in the CK1BD, CK1BD-A and CK1BD-B, that have distinct roles in controlling CK1δ-binding and kinase activity in vitro. KIN-20 and the LIN-42 CK1BD are required for proper molting timing in vivo, and loss of LIN-42 binding changes KIN-20 subcellular localization. The interactions mirror the central role of a stable circadian PER–CK1 complex in setting a robust ~24-hour period. Hence, our results establish LIN-42/PER – KIN-20/CK1δ/ε as a functionally conserved signaling module of two distinct chronobiological systems.
2025-10-10 | PXD058598 | Pride
Project description:Comparison of miRNA profiles of wildtype and lin-28(n719); lin-46(ma164) Caenorhabditis elegans nematodes at the L1 stage
2012-02-09 | GSE35634 | GEO
Project description:MicroRNA-Directed siRNA Biogenesis in Caenorhabditis elegans
| PRJNA124873 | ENA
Project description:Effect of lin-28 and lin-46 on miRNA profile in late L1 stage Caenorhabditis elegans
| PRJNA152485 | ENA
Project description:We performed ChIP-seq analysis of LIN-42 from extracts obtained from staged late L4 hermaphrodites. We found 413 high confidence peaks that are predominately found at promoter regions and transcription start sites of mRNA and microRNA genes. ChIP assays using a functional GFP tagged transgene of LIN-42 using an anti-GFP antibody, as well as using an antibody raised agans the endogenous LIN-42 protein.
2014-06-03 | E-GEOD-58171 | biostudies-arrayexpress