Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1283963 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Caenorhabditis elegans Raw sequence reads-Evaluation of chemotherapeutic agent oxaliplatin-induced germ-cell mutagenesis in alternative in vivo model Caenorhabditis elegans
| PRJNA938168 | ENA
Project description:Evaluation of chemotherapeutic agent oxaliplatin-induced germ-cell mutagenesis in alternative in vivo model Caenorhabditis elegans
| PRJNA937789 | ENA
Project description:Caenorhabditis elegans Raw sequence reads-Evaluation of chemotherapeutic agent Flame retardant of TBBPA, TCEP, TCPP which can induce germ-cell mutagenesis in alternative in vivo model Caenorhabditis elegans
| PRJNA961683 | ENA
Project description:Raw sequence reads Evaluation of chemotherapeutic agent oxaliplatin-induced germ-cell mutagenesis in alternative in vivo model Caenorhabditis elegans
| PRJNA937857 | ENA
Project description:Caenorhabditis elegans Raw sequence reads-Evaluation of heavy metal of potassium dichromate, cadmium chloride, sodium arsenite which can induce germ-cell mutagenesis in alternative in vivo model Caenorhabditis elegans
| PRJNA1005024 | ENA
Project description:The Cell Division Cycle and Apoptosis Regulator (CCAR) protein family members have recently emerged as regulators of alternative splicing and transcription, as well as having other key physiological functions. For example, mammalian CCAR2/DBC1 forms a complex with the zinc factor protein ZNF326 to integrate alternative splicing with RNA polymerase II transcriptional elongation in AT-rich regions of the DNA. Additionally, Caenorhabditis elegans CCAR-1, a homolog to mammalian CCAR2, facilitates the alternative splicing of the perlecan unc-52 gene. However, much about the CCAR family's role in alternative splicing is unknown. We are interested in uncovering the role of the CCAR family in alternative splicing in vivo using Caenorhabditis elegans. We examined the role of CCAR-1 in genome-wide alternative splicing and identified new alternative splicing targets of CCAR-1 using RNA sequencing. Also, we found that CCAR-1 interacts with the spliceosome factors UAF-1 and UAF-2 using mass spectrometry, and that knockdown of ccar-1 affects alternative splicing patterns, motility, and proteostasis of UAF-1 mutant worms. Collectively, we demonstrate a role for CCAR-1 in the regulation of global alternative splicing in C. elegans and in conjunction with UAF-1
2024-02-26 | PXD043100 | Pride
Project description:we used Caenorhabditis elegans as a model organism, to investigate the effect of mannose on the lifespan. Using nematode RNAi methods, RT-PCR, RNA-seq and other experimental method, we explored the possible mechanism for how mannose change the lifespan of Caenorhabditis elegans.
2023-09-01 | GSE192579 | GEO
Project description:Post-transcriptional control of mRNAs by RNA-binding proteins (RBPs) has a prominent role in the regulation of gene expression. RBPs interact with mRNAs to control their biogenesis, splicing, transport, localization, translation, and stability. Defects in such regulation can lead to a wide range of human diseases from neurological disorders to cancer. Many RBPs are conserved between Caenorhabditis elegans and humans, and several are known to regulate apoptosis in the adult C. elegans germ line. How these RBPs control apoptosis is, however, largely unknown. Here, we identify mina-1(C41G7.3) in a RNA interference-based screen as a novel regulator of apoptosis, which is exclusively expressed in the adult germ line. The absence of MINA-1 causes a dramatic increase in germ cell apoptosis, a reduction in brood size, and an impaired P granules organization and structure. In vivo crosslinking immunoprecipitation experiments revealed that MINA-1 binds a set of mRNAs coding for RBPs associated with germ cell development. Additionally, a system-wide analysis of a mina-1 deletion mutant compared to wild type, including quantitative proteome and transcriptome data, hints to a post-transcriptional regulatory RBP network driven by MINA-1 during germ cell development in C. elegans. In particular, we found that the germline-specific Argonaute WAGO-4 protein levels are increased in the mina-1 mutant background. Phenotypic analysis of double mutant mina-1;wago-4 revealed that contemporary loss of MINA-1 and WAGO-4 strongly rescues the phenotypes observed in the mina-1 mutant background. To strengthen this functional interaction, we found that upregulation of WAGO-4 in mina-1 mutant animals causes hypersensitivity to exogenous RNAi. Our comprehensive experimental approach allowed us to describe a phenocritical interaction between two RBPs controlling germ cell apoptosis and exogenous RNAi. These findings broaden our understanding of how RBPs can orchestrate different cellular events such as differentiation and death in C. elegans.
2021-09-08 | PXD011625 | Pride