Heteractis aurora
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1138220 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| SRR30715363_1.fastq.gz | Fastqsanger.gz | |||
| SRR30715363_2.fastq.gz | Fastqsanger.gz |
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Project description:Heteractis magnifica Transcriptome or Gene expression
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Project description:The goal of this study is to identify the effect of inhibition of Aurora-A kinase activity on gene expression and RNA splicing. The perturbation of Aurora-A is well known to affect cell cycle distribution. Therefore, we coupled the inhibition of Aurora-A with cell synchronization procedure in order to avoid the indirect effect of cell cycle perturbation on splicing changes. The mRNA -seq libraries were prepared and subjected to paired-end sequencing on Illumina HiSeq 2500 lanes. Differential gene expression and splicing analysis were carried using the edgeR tool and VAST-tools respectively. The RNA seq analysis identified that pharmacological inhibition of Aurora-A affects alternative splicing of 505 genes while having a marginal effect on gene expression. Overall our work identified Aurora-A as a novel splicing kinase and for the first time, describes a broad role of Aurora-A in regulating alternative splicing.
2024-11-21 | GSE160733 | GEO
Project description:Genome-wide distribution of proteins and histone marks in CD43 negative mouse resting B cells ChIP-seq analyses of Aurora B, Ring1B, Bcx7, USP16, H3K27me3, and Ezh2 were carried out on wild-typeCD43 negative resting B cells. ChIP-seq datasets obtained from Aurora B knockout and RingiB knockout cells were used as negative controls to validate the signals for Aurora B and Ring1B from wild-type cells. 8WG16 ChIP-seq datasets were generated from WT (Cre-ERt2 homozygous) and Ring1B KO (Cre-ERt2/Rnf2 flox homozygous). RNAP-S5ph ChIP-seq datasets were generated from WT (Cre-ERt2 homozygous) and Aurkb KO (Cre-ERt2/Aurkb flox homozygous). ChIP-seq analyses of H3S28 phosphorylation (H3S28ph) and H2AK119 monoubiquitination (H2Aub1) in wild-type (Cre-ERt2 homozygous) and Aurora B KO (Cre-ERt2/Aurkb flox homozygous) CD43 negative resting B cells treated with 250nM tamoxifen (4-hydroxytamoxifen) for 48 hours. ChIP-seq analyses of the levels of unphosphorylated RNA Pol II (8WG16) and serine 5-phosphorylated RNA Pol II (RNAP-S5ph) were conducted in Aurkb KO (Cre-ERt2/Aurkb flox homozygous) and Ring1B KO (Cre-ERt2/Rnf2 flox homozygous) CD43 negative resting B cells treated with 250nM tamoxifen (4-hydroxytamoxifen) for 48 hours respectively). All libraries were prepared from sonicated, formaldehyde-crossilinked chromatin. For H2Aub1, ChIP was performed using micrococcal nuclease-digested, unfixed chromatin, instead.
2013-09-27 | E-GEOD-42705 | biostudies-arrayexpress
Project description:The cell cycle regulator Aurora-A kinase presents an attractive target for cancer therapies, though its inhibition is also associated with toxic side effects. To gain a more nuanced understanding of Aurora-A function, we applied shotgun proteomics to identify 407 specific protein partners, including several splicing factors. Supporting a role in alternative splicing, we found that Aurora-A localizes to nuclear speckles, the storehouse of splicing proteins. Aurora-A interacts with and phosphorylates splicing factors both in vitro and in vivo, suggesting that it regulates alternative splicing by modulating the activity of these splicing factors. Consistently, Aurora-A inhibition significantly impacts the alternative splicing of 505 genes, with RNA motif analysis revealing an enrichment for Aurora-A interacting splicing factors. Additionally, we observed a significant positive correlation between the splicing events regulated by Aurora-A and those modulated by its interacting splicing factors. An interesting example is represented by CLK1 exon 4, which appears to be regulated by Aurora-A through SRSF3. Collectively, our findings highlight a broad role of Aurora-A in the regulation of alternative splicing.
2024-12-10 | GSE281881 | GEO