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Next Generation Sequencing Analysis of Wild Type and SRSF10-/- embryonic day 13.5 heart Transcriptomes

ABSTRACT: We generated the SRSF10 -/- mice, and collected their embryonic heart at 13.5 and controls. Then, we extracted RNAs of embryonic heart and performed next generation sequencing. By comparing sequcing data from WT and SRSF10 -/- samples, we profiled the alternative splicing events and gene expression regulated by SRSF10 during mouse heart development process. E13.5 embryonic heart mRNA profiles of wild type (WT) and SRSF10-/- mice were generated by deep sequencing, using Illumina HiSeq2000.

ORGANISM(S): Mus musculus

SUBMITTER: Ning Wei

PROVIDER: E-GEOD-66965 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Next Generation Sequencing Analysis of Wild Type and SRSF10-/- embryonic day 13.5 heart Transcriptomes

Project description:We generated the SRSF10 -/- mice, and collected their embryonic heart at 13.5 and controls. Then, we extracted RNAs of embryonic heart and performed next generation sequencing. By comparing sequcing data from WT and SRSF10 -/- samples, we profiled the alternative splicing events and gene expression regulated by SRSF10 during mouse heart development process.

2015-04-01 | GSE66965 | GEO

SRSF10 regulates alternative splicing and is required for adipocyte differentiation.

Project description:During adipocyte differentiation, significant alternative splicing changes occur in association with the adipogenic process. However, little is known about roles played by splicing factors in this process. We observed that mice deficient for the splicing factor SRSF10 exhibit severely impaired development of subcutaneous white adipose tissue as a result of defects in adipogenic differentiation. To identify splicing events responsible for this, RNA-seq analysis was performed using embryonic fibroblast cells. Several SRSF10-affected splicing events that are implicated in adipogenesis have been identified. Skipping of lipin1 exon 7 is controlled by SRSF10-regulated cis-element located in the constitutive exon 8. The activity of this element depends on the binding of SRSF10 and correlates with the relative abundance of lipin1a mRNA. A series of experiments demonstrated that SRSF10 controls the production of lipin1a and thus promotes adipocyte differentiation. Indeed, lipin1a expression could rescue SRSF10-mediated adipogenic defects. Taken together, our results identify SRSF10 as an essential regulator for adipocyte differentiation and also provide new insights into splicing control by SRSF10 in lipin1 pre-mRNA splicing. RNA-seq for wide type (WT) and SRSF10-deficient (KO) mouse MEF cells

2014-05-12 | E-GEOD-54226 | biostudies-arrayexpress

Transcriptome analysis of alternative splicing events regulated by SRSF10 reveals position-dependent splicing modulation.

Project description:Splicing factor SRSF10 is known to function as a sequence-specific splicing activator. Here, we used RNA-seq coupled with bioinformatics analysis to identify the extensive splicing network regulated by SRSF10 in chicken cells. We found that SRSF10 promoted both exon inclusion and exclusion. Functionally, many of SRSF10-verified alternative exons are linked to pathways of stress and apoptosis. Importantly, reconstituted SRSF10 in knockout cells recovered wild-type splicing patterns and considerably rescued the stress-related defects. Together, our results provide mechanistic insight into SRSF10-regulated alternative splicing events in vivo and demonstrate that SRSF10 plays a crucial role in cell survival under stress conditions. RNA-seq for wide type (WT) and SRSF10-deficient (KO) chicken DT40 cells

2014-01-22 | E-GEOD-53354 | biostudies-arrayexpress

SRSF10 regulates alternative splicing and is required for adipocyte differentiation.

2014-05-12 | GSE54226 | GEO

Transcriptome analysis of alternative splicing events regulated by SRSF10 reveals position-dependent splicing modulation.

2014-01-22 | GSE53354 | GEO

SRSF10 regulates proliferation of neural progenitor cells and affects neurogenesis in the developing mouse neocortex

Project description:To identify the potential functions of SRSF10 in neural progenitor cells and neocortex development, we constructed SRSF10 flox/flox mice, and conditionally knock out the SRSF10 in the neural progenitor cells by breeding with Nestin-Cre mice.

2023-05-30 | GSE225647 | GEO

Targeting the splicing factor SRSF10 in mouse HCC tumors shapes tumor immunity and immunotherapy

Project description:The efficacy of immune checkpoint blockade (ICB) therapy in hepatocellular carcinoma (HCC) patients remains poor. This article aims to uncover the role and mechanism of SRSF10 in HCC immunotherapy. SRSF10 is upregulated in a variety of tumors and is associated with poor prognosis. SRSF10 binds to the 3’UTR region of MYB and enhances the stability of MYB RNA levels. This activation leads to increased transcriptional expression of key enzymes associated with glycolysis, such as GLUT1, HK1, and LDHA, resulting in higher lactate content in tumor cells. The lactate in tumor cells inside can increase histone lactylation so as to upregulated the expression of SRSF10. Besides, the lactate produced by tumors promotes lactylation of the histone H3K18la site upon transport into macrophages, which could activate transcription of M2 macrophage genes and increase protumour macrophage activity, so as to creating a suppressive immune microenvironment. Clinically, SRSF10 can be utilized as a biomarker to assess the resistance to immunotherapy in different types of solid tumors. The pharmacological targeting of SRSF10 with 1C8 has been shown to be effective in both murine and human preclinical models. In conclusion, we prove that the SRSF10/MYB/glycolysis/lactate axis is critical for triggering immune evasion and anti-PD-1 resistance.

2024-08-18 | GSE273080 | GEO

The regulation of transcriptome in HCC cells by SRSF10 [Huh7_shSRSF10_RNAseq]

Project description:We investigated the impact of SRSF10 knockdown on transcriptome in HCC cells through RNA-seq assays

2024-07-21 | GSE272166 | GEO

A novel class of CLK inhibitors that targets SRSF10 and promote p53-mediated cytotoxicity on human colorectal cancer cells

Project description:The expression of the splicing regulator SRSF10 is elevated in metastatic colorectal cancer (CRC) where it promotes the production of the pro-tumorigenic Bclaf1-L splice variant. We discovered a group of small molecules with an aminothiazole carboxamide core (GPS167, GPS192 and others) that decrease production of Bclaf1-L. Additional alternative splicing events regulated by SRSF10 in HCT116 cells were affected by GPS167/192 (e.g. Mdm4 and Wtap), and other events also shifted in a SRSF10-independent manner (e.g. Mdm2, Nab2, Tra2a). GPS167/192 increased the interaction of SRSF10 with CLK1 and CLK4 kinases, leading us to show that GPS167/192 were CLK kinase inhibitors impacting the activity of SRSF10. Notably, GPS167 impaired the growth of colorectal cancer cell lines and organoids, inhibited anchorage-independent colony formation, cell migration and promoted cytoxicity that required SRSF10 and p53. The anti-cancer potential of this new class of CLK kinase inhibitors is further supported by the observation that GPS167 only minimally affected normal colonocytes and normal colorectal organoids. Thus, while SRSF10 promotes tumorigenesis, DNA damage promoted by GPS167 redirects SRSF10 activity towards cell death in a p53-dependent manner.

2020-06-30 | GSE153492 | GEO

A novel class of CLK kinases inhibitors that target SRSF10 and promote p53-mediated cytotoxicity on human colorectal cancer cells

Project description:The elevated expression of the splicing regulator SRSF10 in metastatic colorectal cancer (CRC) stimulates the production of the pro-tumorigenic Bclaf1-L splice variant. We discovered a group of small molecules with an aminothiazole carboxamide core (GPS167, GPS192 and others) that decrease production of Bclaf1-L. While additional alternative splicing events regulated by SRSF10 are affected by GPS167/192 in HCT116 cells (e.g., in MDM4, WTAP, SLK1 and CLK1), other events are shifted in a SRSF10-independent manner (e.g., in MDM2, NAB2 and TRA2A). GPS167/192 increased the interaction of SRSF10 with the CLK1 and CLK4 kinases, leading us to show that GPS167/192 are CLK kinase inhibitors preferentially impacting the activity of SRSF10. Notably, GPS167 impairs the growth of CRC cell lines and organoids, inhibits anchorage-independent colony formation, cell migration, and promotes cytoxicity that requires SRSF10 and p53. In contrast, GPS167 only minimally affects normal colonocytes and normal colorectal organoids. Thus, GPS167 reprograms the tumorigenic activity of SRSF10 in CRC cells to elicit p53-dependent apoptosis.

2021-06-15 | GSE161168 | GEO

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