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Transcriptome profiling of the effects of Aurora B mediated phosphoregulation of CNOT3 in differentiating mesendodermal cells

ABSTRACT: Transcriptome profiling of the effects of Aurora B mediated phosphoregulation of CNOT3 in differentiating mesendodermal cells

PROVIDER: PRJNA575042 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10207407_1.fastq.gz	Fastqsanger.gz
	SRR10207407_2.fastq.gz	Fastqsanger.gz
	SRR10207408_1.fastq.gz	Fastqsanger.gz
	SRR10207408_2.fastq.gz	Fastqsanger.gz
	SRR10207409_1.fastq.gz	Fastqsanger.gz

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Transcriptome profiling of the effects of Aurora B mediated phosphoregulation of CNOT3 in differentiating mesendodermal cells

Project description:Characterization of the transcriptome profile of CNOT3 phospho mutants of Aurora B target residues (T292/S294) in mesendoderm differentiated cells

2021-10-04 | GSE138213 | GEO

CNOT3 interacts with the Aurora B and MAPK/ERK kinases to promote survival of differentiating mesendodermal progenitor cells.

Project description:Mesendoderm cells are key intermediate progenitors that form at the early primitive streak (PrS) and give rise to mesoderm and endoderm in the gastrulating embryo. We have identified an interaction between CNOT3 and the cell cycle kinase Aurora B that requires sequences in the NOT box domain of CNOT3 and regulates MAPK/ERK signaling during mesendoderm differentiation. Aurora B phosphorylates CNOT3 at two sites located close to a nuclear localization signal and promotes localization of CNOT3 to the nuclei of mouse embryonic stem cells (ESCs) and metastatic lung cancer cells. ESCs that have both sites mutated give rise to embryoid bodies that are largely devoid of mesoderm and endoderm and are composed mainly of cells with ectodermal characteristics. The mutant ESCs are also compromised in their ability to differentiate into mesendoderm in response to FGF2, BMP4, and Wnt3 due to reduced survival and proliferation of differentiating mesendoderm cells. We also show that the double mutation alters the balance of interaction of CNOT3 with Aurora B and with ERK and reduces phosphorylation of ERK in response to FGF2. Our results identify a potential adaptor function for CNOT3 that regulates the Ras/MEK/ERK pathway during embryogenesis.

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Gene expression profile of Cnot3(+/+) & Cnot3 (∆/∆) pro-B cells

Project description:To study the role Cnot3 in early B cells development, RNASeq analysis of pro-B cells (B220+ and CD43+) was performed in tamoxifen treated Cnot3(fl/fl) RERTCre and Cnot3+/+;RERTCre mice.

2016-11-21 | GSE87635 | GEO

Transcriptome wide analysis of Cnot3 target mRNA in mouse hearts

Project description:Through RNA immunoprecipitation with anti-Cnot3 antiboy from mouse heart lysates and RNA-seq (Cnot3 RIP-seq) and gene ontology analyses, we show the comprehensive picute of cardiac Cnot3 target genes.

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Regulation of B cell early development by CNOT3

Project description:The CCR4-NOT complex, bearing poly(A) deadenylation activity, is a highly conserved regulator that is involved in biological control; however its action mechanisms and physiological targets remain unclear. Using genetic deletion of the CNOT3 subunit of this complex in early B cell progenitors, we show that CNOT3 plays a critical role in pro- to pre-B cell transition. CNOT3 participated in controlling germline transcription, compaction of the immunoglobulin heavy chain (Igh) locus, and Igh rearrangement, and in destabilizing tumor suppressor p53 mRNA. Moreover, by genetic ablation of p53 or introduction of pre-rearranged Igh transgene, the B cell developmental defect in the Cnot3 knockout background could be partly rescued, suggesting that CCR4-NOT complex exerts critical control in B cell differentiation processes by co-utilizing transcriptional and post-transcriptional mechanisms. Pro-B cells mRNA profiles of Mb1(cre/+) and Cnot3(fl/fl)Mb1(cre/+) mice were generated by deep sequencing using Illumina HiSeq 1500

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Proteomic study identifies Aurora-A mediated regulation of alternative splicing through multiple splicing factors

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.

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Expression data from the liver of wild-type and Cnot3+/- mice: Fasted

Project description:Decay of mRNAs initiates with shortening of the poly(A) tail. Although the CCR4-NOT complex participates in deadenylation, how it becomes activates remain obscure. We show that complete deficiency in CNOT3, subunit 3 of this complex, is lethal in mice, but that heterozygotes survive as lean mice with hepatic and adipose tissues containing reduced lipid levels. Cnot3+/- mice have enhanced metabolic rates and remain lean on high-fat diets. To examine the underlying mechanisms by which CNOT3 is involved in the control of metabolic balance, we compared the gene expression profiles of wild-type and Cnot3+/- mice using Affymetrix microarray technology. We chose to analyze the liver because the CNOT3 level in the liver was affected by the feeding condition and because the liver plays a major role in glucose and lipid metabolism.

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Expression data from the liver of wild-type and Cnot3+/- mice: Fasted

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