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Microbial-ligand independent regulation of lymphpoiesis by NOD1

ABSTRACT: Microbial-ligand independent regulation of lymphpoiesis by NOD1

PROVIDER: PRJNA991463 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25158760.fastq.gz	Fastqsanger.gz
	SRR25158761.fastq.gz	Fastqsanger.gz
	SRR25158762.fastq.gz	Fastqsanger.gz
	SRR25158763.fastq.gz	Fastqsanger.gz
	SRR25158764.fastq.gz	Fastqsanger.gz

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Microbial-ligand independent regulation of lymphpoiesis by NOD1

Project description:Aberrant differentiation of progenitor cells in the hematopoietic system is known to severely impact host immune responsiveness. Here we demonstrate that NOD1, a cytosolic innate sensor of bacterial peptidoglycan, also functions in murine hematopoietic cells as a major regulator of both the generation and differentiation of lymphoid progenitors as well as peripheral T lymphocyte homeostasis. We further show that NOD1 mediates these functions by facilitating STAT5 signaling downstream of hematopoietic cytokines. In steady-state, loss of NOD1 resulted in a modest but significant decrease in numbers of mature T, B and NK cells. During systemic protozoan infection, this defect was markedly enhanced leading to host mortality. Lack of functional NOD1 also impaired T-cell-dependent anti-tumor immunity while preventing colitis. These findings reveal that in addition to its classical role as a bacterial ligand receptor, NOD1 plays an important function in regulating adaptive immunity through interaction with a major host cytokine signaling pathway.

2023-10-25 | GSE236485 | GEO

NLR Nod1 signaling promotes survival of BCR-engaged mature B cells through upregulated Nod1 as a positive outcome

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A modest change in regulation of NOD1 expression has a major impact on inflammation and gastric cancer

Project description:Altered protein dosage by defects in single genes leads to haploinsufficiencies and monogenic disorders, but the impact of small changes in gene expression on multifactorial disease is unknown. Here we show that a persistent small increase in expression of NOD1, a key innate sensor of bacterial infection, precipitates a large physiological effect with dramatically altered cellular function associated with carcinogenesis. Inhibition of miR-15b and miR-16 microRNA function leads to a ~1.2-1.4 fold increase in NOD1 protein concentration, with even slightly greater increases leading to ligand-independent, switch-like NOD1 activation. miRNA regulation of NOD1 is impaired in gastric cancer with a small increase being associated with greater early disease mortality. Overall, our data show that tight control of NOD1 expression by miRNA prevents this sensor from exceeding a physiological switching checkpoint that promotes persistent inflammation and lethal cancer progression, and reveal the impact of a single and modest cellular alteration on cancer.

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Zebrafish embryos microinjected with ptGFP1 (control group) or ptGFP1-NOD1 (NOD1 group)

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Gene expression in aortic roots of Apoe KO mice with Nod1 stimulation

Project description:To explore the mechanisms underlying progression of atherosclerosis provoked by Nod1 ligand stimulation, we performed microarray gene expression profiling of aortic roots of 6- and 9-week-old Apoe KO mice with or without oral FK565 administration. A gene ontology analysis of the genes up-regulated in FK565-administrated group at both time points showed that a number of biological process terms were associated with immune response. Among chemokine/cytokine genes, we observed that only 3 genes such as Ccl5, Ccl8 and Cxcl16 elevated more than 2-fold in response to oral administration of FK565 at both time points. An eight chip study using total RNA recovered from aortic roots in Apoe KO mice with or without FK565 administration, at the age of 6 and 9 weeks. Two independent experiments were performed in each group. In FK565-administrated groups, mice were orally administrated FK565 (50 µg) twice a week for 1 or 4 weeks from 5 weeks of age.

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Gene expression in fetal aortic arteries of C57BL/6 mice with Nod1 stimulation

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Luminal lncRNAs Regulation by ERα-controlled Enhancers in a Ligand-independent Manner in Breast Cancer Cells

Project description:Luminal lncRNAs Regulation by ERα-controlled Enhancers in a Ligand-independent Manner in Breast Cancer Cells

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Unique Ligand and Kinase-Independent Roles of the Insulin Receptor in Regulation of Cell Cycle, Senescence and Apoptosis

Project description:Insulin acts through the insulin receptor (IR) tyrosine kinase to exert its classical metabolic and mitogenic actions. Here, using receptors with either short or long deletion of the β-subunit or mutation of the kinase active site (K1030R, we uncover a second novel IR signaling pathway that is intracellular domain dependent, but ligand and tyrosine kinase-independent (LYK-I). These LYK-I actions of the IR are linked to changes in phosphorylation of a network of proteins involved in the regulation of extracellular matrix organization, cell cycle, ATM signaling and cellular senescence; and result in upregulation of expression of multiple extracellular matrix-related genes and proteins, down-regulation of immune/interferon-related genes and proteins, and increased sensitivity to apoptosis. Thus, in addition to classical ligand and tyrosine kinase-dependent (LYK-D) signaling, the IR regulates a second, novel ligand and tyrosine kinase-independent (LYK-I) pathway which regulates the cellular machinery involved in senescence, matrix interaction and response to extrinsic challenges.

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