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Hypoxia-driven deSUMOylation of EXOSC10 promotes adaptive changes in the transcriptome profile

ABSTRACT: Hypoxia-driven deSUMOylation of EXOSC10 promotes adaptive changes in the transcriptome profile

PROVIDER: PRJNA956549 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24196150.fastq.gz	Fastqsanger.gz
	SRR24196151.fastq.gz	Fastqsanger.gz
	SRR24196152.fastq.gz	Fastqsanger.gz
	SRR24196153.fastq.gz	Fastqsanger.gz
	SRR24196158.fastq.gz	Fastqsanger.gz

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Similar Datasets

Hypoxia-driven deSUMOylation of EXOSC10 promotes adaptive changes in the transcriptome profile

Project description:Reduced oxygen availability (hypoxia) triggers adaptive cellular responses via hypoxia-inducible factor (HIF)-dependent transcriptional activation. Adaptation to hypoxia also involves transcription-independent processes like post-translational modifications, however these mechanisms are poorly characterized. Investigating the involvement of protein SUMOylation in response to hypoxia, we discovered that hypoxia strongly decreases the SUMOylation of Exosome subunit 10 (EXOSC10), the catalytic subunit of the RNA exosome, in a HIF-independent manner. EXOSC10 is a multifunctional exoribonuclease enriched in the nucleolus that mediates the processing and degradation of various RNA species. We demonstrate that the Ubiquitin-specific protease 36 (USP36) SUMOylates EXOSC10 and we reveal SUMO1/sentrin-specific peptidase 3 (SENP3) as the enzyme mediating deSUMOylation of EXOSC10. Under hypoxia, EXOSC10 dissociates from USP36 and translocates from the nucleolus to the nucleoplasm concomitant with its deSUMOylation. Loss of EXOSC10 SUMOylation does not detectably affect rRNA maturation but affects the mRNA transcriptome by modulating the expression levels of hypoxia-related genes. Our data suggest that dynamic modulation of EXOSC10 SUMOylation and localization under hypoxia regulates the RNA degradation machinery to facilitate cellular adaptation to low oxygen conditions.

2024-01-30 | GSE229894 | GEO

Hypoxia-driven deSUMOylation of EXOSC10 promotes adaptive changes in the transcriptome profile.

Project description:Reduced oxygen availability (hypoxia) triggers adaptive cellular responses via hypoxia-inducible factor (HIF)-dependent transcriptional activation. Adaptation to hypoxia also involves transcription-independent processes like post-translational modifications; however, these mechanisms are poorly characterized. Investigating the involvement of protein SUMOylation in response to hypoxia, we discovered that hypoxia strongly decreases the SUMOylation of Exosome subunit 10 (EXOSC10), the catalytic subunit of the RNA exosome, in an HIF-independent manner. EXOSC10 is a multifunctional exoribonuclease enriched in the nucleolus that mediates the processing and degradation of various RNA species. We demonstrate that the ubiquitin-specific protease 36 (USP36) SUMOylates EXOSC10 and we reveal SUMO1/sentrin-specific peptidase 3 (SENP3) as the enzyme-mediating deSUMOylation of EXOSC10. Under hypoxia, EXOSC10 dissociates from USP36 and translocates from the nucleolus to the nucleoplasm concomitant with its deSUMOylation. Loss of EXOSC10 SUMOylation does not detectably affect rRNA maturation but affects the mRNA transcriptome by modulating the expression levels of hypoxia-related genes. Our data suggest that dynamic modulation of EXOSC10 SUMOylation and localization under hypoxia regulates the RNA degradation machinery to facilitate cellular adaptation to low oxygen conditions.

| S-EPMC10817850 | biostudies-literature

RNA binding by Exosc10 in the developing mouse cortex

Project description:In our RIP-seq experiment, RNAs were purified from the E12.5 WT mouse cortex. By sequencing of the Exosc10-bound RNAs, binding enrichment of Exosc10 on 3159 transcripts was identified (adjusted p-value < 0.05). GO analysis revealed that the Exosc10-bound transcripts participate in various processes of brain development.

2021-01-20 | GSE164188 | GEO

The Ubiquitin-Specific Protease USP36 SUMOylates EXOSC10 and promotes the nucleolar RNA exosome function in rRNA processing

Project description:The RNA exosome is an essential 3’ to 5’ processing exoribonuclease complex that mediates degradation, processing, and quality control of virtually all eukaryotic RNAs. The nucleolar RNA exosome, consisting of a 9-subunit core and a distributive 3ʹ to 5ʹ exonuclease EXOSC10, plays a critical role in processing and degrading nucleolar RNAs, including pre-ribosomal RNA (pre-rRNA). However, how the RNA exosome is regulated in the nucleolus is poorly understood. Here, we report that the nucleolar ubiquitin-specific protease USP36 is a novel regulator of the nucleolar RNA exosome. USP36 binds to the RNA exosome through direct interaction with EXOSC10. Interestingly, USP36 does not significantly regulate the levels of EXOSC10 and other exosome subunits. Instead, it mediates EXOSC10 SUMOylation at Lys (K) 583. Mutating K583 impaired the binding of EXOSC10 to pre-rRNAs and the K583R mutant failed to rescue the defects in rRNA processing and cell growth inhibition caused by knockdown of endogenous EXOSC10, indicating that EXOSC10 SUMOylation is critical for the exosome function in rRNA processing. Furthermore, USP36 itself is a rRNA-binding protein that associates pre-rRNA. These results suggest that USP36 acts as a novel SUMO ligase to mediate EXOSC10 SUMOylation critical for the RNA exosome function in rRNA processing and ribosome biogenesis.

2023-07-20 | PXD031592 | Pride

Nutrient-driven dedifferentiation of enteroendocrine cells promotes adaptive intestinal growth

Project description:Nutrient-driven dedifferentiation of enteroendocrine cells promotes adaptive intestinal growth

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Attenuating Hypoxia Driven Malignant Behavior in Glioblastoma with a Novel Hypoxia-Inducible Factor 2 Alpha Inhibitor

Project description:Attenuating Hypoxia Driven Malignant Behavior in Glioblastoma with a Novel Hypoxia-Inducible Factor 2 Alpha Inhibitor

2020-09-10 | GSE147595 | GEO

RNA-seq of shRNA-mediated EXOSC10 and XRN2 knockdown

Project description:To identify changes in gene expression following EXOSC10 and XRN2 silencing, 3'-end RNA-sequencing was performed on RNA extracted from shEXOSC10 and shXRN2 cells.

2019-12-26 | GSE130865 | GEO

EXOSC10 sculpts the transcriptome during oocyte growth-to-maturation transition

Project description:Growing mammalian oocytes accumulate substantial amounts of RNA, most of which are degraded during the subsequent maturation stage. The growth-to-maturation transition begins with germinal vesicle breakdown (GVBD, envisioned as nuclear envelope breakdown) and is critical for oocyte quality. However, the concomitant changes in the transcriptome during GVBD as well as the underlying machinery remained unclear. Here, we report that an RNA exosome-associated RNase, EXOSC10, sculpts the transcriptome at multiple level to facilitate the oocyte growth-to-maturation transition. We establish an oocyte-specific knockout of Exosc10 in mice using CRISPR/Cas9 and find female subfertility due to failed GVBD. By performing single oocyte RNA-seq in different ways, we document dysregulated transcriptomes, unsuccessfully processed rRNAs in mutant oocytes, and many up-regulated RNAs that encode proteins important for endomembrane trafficking, meiotic cell cycle and RNA metabolism. EXOSC10-depleted oocytes have impaired endomembrane components including endosome, lysosome, ER and Golgi. In addition, CDK1 fails to be activated possibly due to persistent WEE1 activity, which blocked lamina phosphorylation and disassembly in mutant oocytes. Collectively, we propose that EXOSC10 promotes the growth-to-maturation transition in mouse oocytes by degrading mRNAs that encode growth-phase factors and sculpting the transcriptome to support the maturation phase of oogenesis.

2019-11-30 | GSE141190 | GEO

Hypoxia-driven alterations in the B16 melanoma cell transcriptome account for a higher metastatic potential

Project description:Hypoxia-driven alterations in the B16 melanoma cell transcriptome account for a higher metastatic potential: evidence for a role of Ero1L We analyzed transcriptomic adaptations to hypoxia/reoxygenation in B16 melanoma cells. By Ero1L over- and down-expression in vivo, we identified this ER oxidase as an actor of tumor growth and metastasis take. In vitro culture of B16 submitted to hypoxia (oxygen rate less than 1%)

2013-08-01 | E-GEOD-14727 | biostudies-arrayexpress

Nutrient-driven dedifferentiation of enteroendocrine cells promotes adaptive intestinal growth

Project description:Post-developmental organ resizing improves organismal fitness under constantly changing nutrient environments. Although stem cell abundance is a fundamental determinant of adaptive resizing, our understanding of its underlying mechanisms remains primarily limited to the regulation of stem cell division. Here, we demonstrate that nutrient fluctuation induces dedifferentiation in the Drosophila adult midgut to drive adaptive intestinal growth. From lineage tracing and single-cell RNA sequencing, we identify a subpopulation of enteroendocrine (EE) cells that convert into functional intestinal stem cells (ISCs) in response to dietary glucose and amino acids by activating the JAK-STAT pathway. Genetic ablation of EE-derived ISCs severely impairs ISC expansion and midgut growth despite the retention of resident ISCs, and in silico modeling further indicates that EE dedifferentiation enables an efficient increase in the midgut cell number while maintaining epithelial cell composition. Our findings identify a physiologically induced dedifferentiation that ensures ISC expansion during adaptive organ growth in concert with nutrient conditions.

2023-08-12 | GSE207662 | GEO

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