Dataset Information

A549 overexpressing CCAR1 LC-MS/MS

ABSTRACT: CCAR1 mRNA have two transcripts, the 3.5 kb full length transcript and the 2.5 kb shorter transcript which contained a deletion in exon 15—exon 22 of full-length CCAR1 cDNA, where sequences mapped to 1196–3120 bp were missed. CCAR1L and CCAR1S shared a common N-terminus and a common C-terminal end, but the latter had a deletion of SAP domain. As a DNA/RNA-binding domain, the SAP motif is involved in chromosomal organization and apoptosis. To explaine the divergence of CCAR1L and CCAR1S in regulating apoptosis,we purified CCAR1L and CCAR1S from flag-CCAR1L or CCAR1S overexpressing A549 cells by performing IP-MS to screening the possible proteins which are specifically interacting with CCAR1L or CCAR1S.

INSTRUMENT(S): Q Exactive

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Epithelial Cell, Cell Culture

DISEASE(S): Polycystic Kidney,Disease Free

SUBMITTER: Huang Qingyang

LAB HEAD: Zhang Lingqiang

PROVIDER: PXD009266 | Pride | 2018-05-15

REPOSITORIES: Pride

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Publications

Mutually exclusive acetylation and ubiquitylation of the splicing factor SRSF5 control tumor growth.

Chen Yuhan Y Huang Qingyang Q Liu Wen W Zhu Qiong Q Cui Chun-Ping CP Xu Liang L Guo Xing X Wang Ping P Liu Jingwen J Dong Guanglong G Wei Wenyi W Liu Cui Hua CH Feng Zhichun Z He Fuchu F Zhang Lingqiang L

Nature communications 20180625 1

Most tumor cells take up more glucose than normal cells. Splicing dysregulation is one of the molecular hallmarks of cancer. However, the role of splicing factor in glucose metabolism and tumor development remains poorly defined. Here, we show that upon glucose intake, the splicing factor SRSF5 is specifically induced through Tip60-mediated acetylation on K125, which antagonizes Smurf1-mediated ubiquitylation. SRSF5 promotes the alternative splicing of CCAR1 to produce CCAR1S proteins, which pro ...[more]

PMID: 29942010

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Project description:Long non-coding RNAs are often not conserved and their specific functions remain enigmatic. Our studies identify independent and opposing roles for two neural-specific and differentially expressed non-coding RNAs derived from the same locus: the evolutionarily conserved lncRNA Rncr3 and the embedded microRNA miR124a-1. In this study, we found that Rncr3 is expressed in and necessary for embryonic neuroepithelial progenitor proliferation and survival whereas miR124a expression initiates at the onset of and promotes neuronal differentiation. Exons 2 and 3 are also highly conserved between mouse lncRncr3 and human RNCR3. We used CRISPR/Cas9 gene editing of NE-4C cells, a neuroepithelial progenitor cell line from cerebral vesicles of embryonic day 9 (E9) mouse embryos, to create full-length deletion of the Rncr3-miR124a locus (exons 1-4) and specifically delete conserved exons 2 and 3. Both knock-out (KO) and exon2/3 deletion reduced proliferation and increased apoptosis. To comprehensively evaluate the effects of full-length Rncr3-miR124a KO and exons 2/3 deletion, we performed RNA-seq. Genes whose expression was consistently up- or down-regulated in full-length KO and exons 2/3 deletion clones relative to wildtype were aimed. Gene ontology (GO) functional annotation showed enrichment for negative regulation of cell proliferation; cell fate commitment; cell cycle arrest; negative regulation of apoptotic process. We also found that expression of miR124a encoded in exon 4 is limited by Rncr3 conserved exons 2 and 3. The RNA-seq data showed that the GO Biological Process (BP) enrichment of genes significantly upregulated in exons 2/3 deletion cells but not significantly changed in full-length deletion cells (where miR124a is deleted, and hence more similar to wildtype proliferating NPCs with very low miR124a expression) are associated with neuronal differentiation, consistent with miR124a function in differentiation. Our studies illustrate that two non-coding RNAs, Rncr3 and miR124a, are differentially generated from the same primary transcript and have opposing functions in NPC maintenance versus promotion of neuronal differentiation.

Dataset Information

A549 overexpressing CCAR1 LC-MS/MS

Publications

Mutually exclusive acetylation and ubiquitylation of the splicing factor SRSF5 control tumor growth.

Similar Datasets

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