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RNA-seq of Srsf10-KD or control liver samples after feeding with HFD.

ABSTRACT: RNA-seq of Srsf10-KD or control liver samples after feeding with HFD.

PROVIDER: PRJNA745985 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15108177_1.fastq.gz	Fastqsanger.gz
	SRR15108177_2.fastq.gz	Fastqsanger.gz
	SRR15108178_1.fastq.gz	Fastqsanger.gz
	SRR15108178_2.fastq.gz	Fastqsanger.gz
	SRR15108179_1.fastq.gz	Fastqsanger.gz

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RNA-seq of Srsf10-KD or control liver samples after feeding with HFD.

Project description:RNA processing is dysregulated in the liver during the early stages of diet induced liver disease and obesity. Furthermore SR proteins are dysregulated as well. In order to look at the contribution of reduced SRSF10 levels in obesity and liver disease, RNA-seq was performed on liver samples from mice which had been injected with an AAV expressing an shRNA against Srsf10 or luciferase and subsequently fed a HFD for 12 weeks.

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Phosphoribotrap-based profiling of activated hypothalamic cells during acute high-fat diet (HFD)-feeding

Project description:To identify novel neurocircuits activated upon short-term HFD feeding, we employed phosphoribotrap-profiling, which allows for the unbiased identification of alterations in neuronal activation via immunoprecipitation of phosphorylated S6 ribosomal protein-tagged ribosomes from hypothalamic extracts of mice exposed to either 3 days of normal chow diet or HFD-feeding. We have analyzed mRNA selectively expressed in hypothalamic cells activated by a either normal chow diet (NCD)-feeding for 3 days or high fat diet (HFD)-feeding for 3 days. 10-week-old male C57/BL6N mice were put either on a normal chow diet or a high fat diet for 3 days. Afterwards, mice were sacrificed by cervical dislocation. The hypothalamus was rapidly dissected using a stainless steel brain matrix and immediately frozen in liquid nitrogen. Hypothalamic tissues were pooled (8 per IP).

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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

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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

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RNA-seq of THP1 cells with SRSF10 knockdown

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