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Xrp1 governs the stress response program to spliceosome dysfunction

ABSTRACT: Xrp1 governs the stress response program to spliceosome dysfunction

PROVIDER: PRJNA838615 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19226386_1.fastq.gz	Fastqsanger.gz
	SRR19226386_2.fastq.gz	Fastqsanger.gz
	SRR19226387_1.fastq.gz	Fastqsanger.gz
	SRR19226387_2.fastq.gz	Fastqsanger.gz
	SRR19226388_1.fastq.gz	Fastqsanger.gz

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Xrp1 governs the stress response program to spliceosome dysfunction

Project description:Xrp1 governs the stress response program to spliceosome dysfunction

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Xrp1 governs the stress response program to spliceosome dysfunction

Project description:Xrp1 governs the stress response program to spliceosome dysfunction

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Xrp1 governs the stress response program to spliceosome dysfunction.

Project description:Co-transcriptional processing of nascent pre-mRNAs by the spliceosome is vital to regulating gene expression and maintaining genome integrity. Here, we show that the deficiency of functional U5 small nuclear ribonucleoprotein particles (snRNPs) in Drosophila imaginal cells causes extensive transcriptome remodeling and accumulation of highly mutagenic R-loops, triggering a robust stress response and cell cycle arrest. Despite compromised proliferative capacity, the U5 snRNP-deficient cells increased protein translation and cell size, causing intra-organ growth disbalance before being gradually eliminated via apoptosis. We identify the Xrp1-Irbp18 heterodimer as the primary driver of transcriptional and cellular stress program downstream of U5 snRNP malfunction. Knockdown of Xrp1 or Irbp18 in U5 snRNP-deficient cells attenuated JNK and p53 activity, restored normal cell cycle progression and growth, and inhibited cell death. Reducing Xrp1-Irbp18, however, did not rescue the splicing defects, highlighting the requirement of accurate splicing for cellular and tissue homeostasis. Our work provides novel insights into the crosstalk between splicing and the DNA damage response and defines the Xrp1-Irbp18 heterodimer as a critical sensor of spliceosome malfunction and mediator of the stress-induced cellular senescence program.

| S-EPMC10954486 | biostudies-literature

Xrp1 governs the stress response program to spliceosome dysfunction

Project description:Unperturbed pre-mRNA splicing is crucial for proper expression of eukaryotic genes, but also maintenance of genome integrity. Loss of splicing factors is associated to DNA damage arising through different mechanisms, among which is the accumulation of mutagenic DNA/RNA hybrids (R-loops). RNase H1 recognizes and degrades the RNA moiety within R-loops, and is a commonly used marker for R-loops. Ecdysoneless protein was previously shown to participate in pre-mRNA splicing through its association with the U5 snRNP. In this study we have performed in vivo Targeted DamID using the Dam-RNase H1 construct to map the localization of R-loops throughout the Drosophila genome in control and Ecd-deficient Drosophila wing imaginal discs.

2024-01-31 | GSE213325 | GEO

Xrp1 governs the stress response program to spliceosome dysfunction

Project description:We investigated the changes in gene expression in response to reduced levels of Ecdysoneless (Ecd), and the role of Xrp1 in induction of transcriptional changes upon loss of Ecd in the developing wing disc of Drosophila. To do this we utilized the GAL4/UAS system to express UAS-ecd-RNAi alone and in combination with UAS-xrp1-RNAi in the nubbin-domain (nub-Gal4, UAS-mRFP, UAS-ecd-RNAi and nub-Gal4, UAS-mRFP, UAS-ecd-RNAi, xrp1-RNAi) of the wing disc and used nub-Gal4, UAS-mRFP wing discs as controls. We quantified transcriptomic expression analysis from four biological replicates for both experimental groups

2024-01-31 | GSE213298 | GEO

Xrp1 governs the stress response program to spliceosome dysfunction

Project description:We investigated the changes in gene expression in response to reduced levels of Ecdysoneless (Ecd) in the developing wing disc of Drosophila. To do this we utilized the GAL4/UAS system to express UAS-ecd-RNAi in the nubbin-domain (nub-Gal4, UAS-mRFP, UAS-ecd-RNAi) of the wing disc and used Nub-Gal4/+ wing discs as controls. We quantified transcriptomic expression analysis from four biological replicates for both experimental groups

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Spliceosome iCLIP

Project description:Spliceosome iCLIP

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Spliceosome iCLIP

Project description:The studies of spliceosomal interactions are challenging due to their dynamic nature. Here we developed spliceosome iCLIP, which immunoprecipitates SmB along with snRNPs and auxiliary RNA binding proteins (RBPs) to simultaneously map the spliceosomal binding to human snRNAs and pre-mRNAs. This identified 9 distinct regions on pre-mRNAs, which overlap with position-dependent binding patterns of 15 RBPs. Using spliceosome iCLIP, we additionally identified >50,000 branchpoints (BPs) that have canonical features, unlike those identified by RNA-seq. The iCLIP BPs generally overlap with the computationally predicted BPs, and alternative BPs are associated with extended regions of structurally accessible RNA. We find that the position and strength of BPs defines the binding patterns of SF3 and U2AF complexes, whereas the RNA structure around BPs affects the sensitivity of exons to perturbation of these complexes. Our findings introduce spliceosome iCLIP as a new method for transcriptomic studies of BPs and splicing mechanisms.

2019-08-30 | E-MTAB-6950 | biostudies-arrayexpress

p53 governs an alveolar type 1 differentiation program in lung cancer suppression

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Interferon Regulatory Factor-8 (IRF8) Expression in Macrophages Governs an Anti-Metastatic Program in Breast Cancer

Project description:High macrophage infiltration in cancer is associated with reduced survival in animal models and in patients. This reflects a shift in the macrophage response from a tumor-suppressive to tumor-supportive program governed by transcriptional events regulated by the inflammatory milieu. Although several transcription factors are known to drive a pro-metastatic program, those that govern an anti-metastatic program are less understood. Interferon regulatory factor-8 (IRF8) is integral for macrophage responses against infections. Using a genetic loss-of-function approach, we tested the hypothesis that IRF8 expression in macrophages governs their capacity to inhibit metastasis. We found that: 1) metastasis was significantly increased in mice with IRF8-deficient macrophages; 2) IRF8-deficient macrophages displayed a neutrophil-like program enriched for metastasis-associated genes; and 3) lower IRF8 expression correlated with reduced survival in human breast cancer and melanoma with high or low macrophage infiltration. These data demonstrate a previously unrecognized role for IRF8 in macrophage biology to control metastasis.

2019-01-28 | GSE116904 | GEO

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