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Cross species transcriptomic signatures predict response to MK2 inhibition in mouse models of chronic inflammation

ABSTRACT: Cross species transcriptomic signatures predict response to MK2 inhibition in mouse models of chronic inflammation

PROVIDER: PRJNA690058 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13367400.fastq.gz	Fastqsanger.gz
	SRR13367500.fastq.gz	Fastqsanger.gz
	SRR13367401.fastq.gz	Fastqsanger.gz
	SRR13367501.fastq.gz	Fastqsanger.gz
	SRR13367402.fastq.gz	Fastqsanger.gz

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Cross species transcriptomic signatures predict response to MK2 inhibition in mouse models of chronic inflammation

Project description:Translating observations from preclinical models to patients is one of the most pressing challenges in biomedical research. Part of the challenge derives from the necessity of studying preclinical therapeutic responses in genetically and environmentally homogenous mouse models, which exhibit less variability than genetically and environmentally heterogeneous humans. This problem is especially relevant for inflammatory bowel diseases (IBD), which are genetically complex and exhibit significant inter-patient heterogeneity in disease presentation and therapeutic response. Here, we show that mouse models of IBD exhibit variable responses to inhibition a MK2, a pro-inflammatory serine/threonine kinase, and that MK2 inhibition suppresses inflammation by targeting inflammatory monocytes and neutrophils. Using a computational approach (TransComp-R) that allows for cross-species comparison of transcriptomic features, we identified an IBD patient subgroup that is predicted to respond to MK2 inhibition and an independent preclinical model of chronic intestinal inflammation predicted to be non-responsive, which we validated experimentally. Thus, cross-species mouse-human translation approaches can help to identify patient subpopulations in which to deploy new therapies.

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Cross-species transcriptomic signatures predict response to MK2 inhibition in mouse models of chronic inflammation.

Project description:Inflammatory bowel diseases (IBDs) are genetically complex and exhibit significant inter-patient heterogeneity in disease presentation and therapeutic response. Here, we show that mouse models of IBD exhibit variable responses to inhibition of MK2, a pro-inflammatory serine/threonine kinase, and that MK2 inhibition suppresses inflammation by targeting inflammatory monocytes and neutrophils in murine models. Using a computational approach (TransComp-R) that allows for cross-species comparison of transcriptomic features, we identified an IBD patient subgroup that is predicted to respond to MK2 inhibition, and an independent preclinical model of chronic intestinal inflammation predicted to be non-responsive, which we validated experimentally. Thus, cross-species mouse-human translation approaches can help to identify patient subpopulations in which to deploy new therapies.

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WT and Mk2/3 KO MEFs response to etoposide

Project description:Primary mouse embryonic fibroblasts (MEFs) from wt and MK2/3 KO mice were treated with 20µM etoposide. Primary MEFs from wt and MK2/3 KO mice were treated with 20µM etoposide and RNA extracted after 1h and 6h.

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Project description:The p38MAPK downstream targets MK 2 and 3 are critical for the regulation of the macrophage response towards bacterial lipopolysaccharid (LPS). The extent these two kinases act cooperatively in regulating LPS-induced inflammatory cytokine expression and their distinct regulatory effects are still unclear. To address this point, whole transcriptome analyses had been performed using bone marrow derived macrophages (BMDM) generated from MK2-/- or MK2/3-/- animals and from wildtype littermates. The BMDM were treated with 100 ng/ml LPS for 360 minutes or with medium as control. Thereafter, total mRNA was isolated and subjected to array analysis using the SurePrint G3 Mouse 8x60K Microarray Kit from Agilent.

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Project description:Ultraviolet (UV) light radiation induces the formation of bulky photoproducts in the DNA that globally affect transcription and splicing. However, the signaling pathways and mechanisms that link UV light-induced DNA damage to changes in RNA metabolism remain poorly understood. Here, we employ quantitative phosphoproteomics and protein kinase inhibition to provide a systems view on protein phosphorylation patterns induced by UV light, and uncover the dependencies of phosphorylation events on the canonical DNA damage signaling by ATM/ATR and the p38 MAP kinase pathway. We identify RNA binding proteins as primary substrates and 14-3-3 as direct readers of p38-MK2-dependent phosphorylation induced by UV light. Mechanistically, we show that MK2 phosphorylates the RNA binding subunit of the NELF complex NELFE on Serine 115. NELFE phosphorylation promotes the recruitment of 14-3-3 and rapid dissociation of the NELF complex from chromatin, which is accompanied by RNA polymerase II elongation.

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Project description:Ultraviolet (UV) light radiation induces the formation of bulky photoproducts in the DNA that interfere with replication and transcription. Recent studies showed that exposure of human cells to UV light globally affects transcription and alternative splicing, however, the signaling pathways and mechanisms that link UV light-induced DNA damage to RNA metabolism regulation remain poorly understood. Here, we provide a systems view on protein phosphorylation patterns induced by UV light, and uncover the dependencies of phosphorylation events on the canonical DNA damage signaling mediated by ATM/ATR or p38 MAP kinase pathway. We identify RNA binding proteins as primary targets and 14-3-3 family as direct readers of p38-MK2-dependent phosphorylation induced by UV light. Moreover, we show that MK2 phosphorylates the RNA binding subunit of the NELF complex NELFE on S115. NELFE phosphorylation promotes the recruitment of 14-3-3 and rapid dissociation of the NELF complex from chromatin that is accompanied with an increase in transcriptional elongation.

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