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RNA-seq of HeLa cells and RPE1 cells after USP39 KD using RNAi

ABSTRACT: RNA-seq of HeLa cells and RPE1 cells after USP39 KD using RNAi

PROVIDER: PRJNA954019 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24120337_1.fastq.gz	Fastqsanger.gz
	SRR24120337_2.fastq.gz	Fastqsanger.gz
	SRR24120338_1.fastq.gz	Fastqsanger.gz
	SRR24120338_2.fastq.gz	Fastqsanger.gz
	SRR24120339_1.fastq.gz	Fastqsanger.gz

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RNA-seq of HeLa cells and RPE1 cells after USP39 KD using RNAi

Project description:We used HeLa cells and RPE1 cells after knockdown (KD) of USP39 using siRNAs. We compared differential expression and alternative splicing between Control and KD cells.

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Complexome profiling of nuclear lysates from control and USP39-depleted HeLa cells

Project description:RNA splicing and protein degradation systems allow the functional adaptation of the proteome in response to changing cellular contexts. However, the regulatory mechanisms connecting these processes remain poorly understood. Here, we show that impaired spliceosome assembly caused by USP39 deficiency leads to a pathogenic splicing profile characterized by the use of cryptic 5′ splice sites. To explore the interactions of USP39 and the effect of its depletion in HeLa cells, we performed complexome profiling of nuclear lysates. We observed most USP39 stably integrated into the tri-snRNP complex and there is almost no free nuclear protein. More importantly, the relative abundance of tri-snRNP spliceosome complex was impaired in USP39-depleted cells. As previous reports indicated, USP39 is a regulator of tri-snRNP stability and its depletion decreased the levels of assembled U4/U6.U5 complexes.

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RNA sequencing of liver tissues from liver-specific Usp39 knockout (Usp39-HKO) mice

Project description:Regulation of alternative splicing (AS) is crucial for gene expression and enables a single transcript to yield multiple isoforms that increase transcriptome and proteome diversity. Dysregulated AS has been linked to the development of non-alcoholic fatty liver diseases (NAFLD). However, the splicing factors involved in hepatic homeostasis and their functional mechanisms remain to be further characterized. Here, we report that spliceosome component Usp39 plays a critical role in the regulation of hepatocyte lipid homeostasis. We found that Usp39 expression is downregulated in hepatic tissues of NAFLD and non-alcoholic steatohepatitis (NASH) subjects. We observed increased lipid accumulation, spontaneous steatosis and impaired autophagy, lipophagy in particular, in mice with hepatocyte-specific Usp39 deletion. Combined analysis of RIP-seq and RNA-seq data revealed that Usp39 regulates AS of several autophagy-related genes including Hsf1. More specifically, deletion of Usp39 resulted in alternative 5’ splice site selection of exon 6 in Hsf1 and consequently reduced expression. Hsf1 was also found to be downregulated in NAFLD/NASH mice and patients. Importantly, overexpression of Hsf1 restored lipophagy, attenuated lipid accumulation and alleviated NASH caused by Usp39 deficiency. Taken together, our findings indicate that Usp39-mediated AS is crucial for sustaining lipophagy and lipid homeostasis in the liver.

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RPE1

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Gene expression in hTERT-RPE1 cells with overexpression of MFRP

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