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Gonadal gap junctions activate Notch signaling to suppress intestinal innate immunity via p38/PMK-1 and lysosome pathway II

ABSTRACT: We showed that the innexin genes encoding gap junction subunits positively regulated GLP-1/Notch signaling to suppress the innate immunity of C. elegans via PMK-1/p38 pathway.

ORGANISM(S): Caenorhabditis elegans

PROVIDER: GSE206126 | GEO | 2025/06/05

REPOSITORIES: GEO

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Gonadal gap junctions activate Notch signaling to suppress intestinal innate immunity via p38/PMK-1 and lysosome pathway

Project description:We showed that the innexin genes encoding gap junction subunits positively regulated GLP-1/Notch signaling to suppress the innate immunity of C. elegans via PMK-1/p38 pathway. The unc-17 acts in the dowmstream of inx-14/glp-1 to regulate innate immunity.

2025-06-14 | GSE206090 | GEO

Gonadal gap junctions activate Notch signaling to suppress intestinal innate immunity via p38/PMK-1 and lysosome pathway

Project description:Gonadal gap junctions activate Notch signaling to suppress intestinal innate immunity via p38/PMK-1 and lysosome pathway

| PRJNA849169 | ENA

Gonadal gap junctions activate Notch signaling to suppress intestinal innate immunity via p38/PMK-1 and lysosome pathway II

Project description:Gonadal gap junctions activate Notch signaling to suppress intestinal innate immunity via p38/PMK-1 and lysosome pathway II

| PRJNA849251 | ENA

Neuronal Acetylcholine Couples Gonadal Gap Junction/Notch Signaling Axis to Gut Defense

Project description:Gap junctions mediate intercellular communications across cellular networks in the nervous and the immune systems, while the role in the intestinal innate immunity is poorly understood. Here, we identified that an innexin gene inx-14 encoding one of heterotypic and heteromeric gap junction subunits acts in the gonad to attenuate the intestinal defense through PMK-1/p38 pathway. The RNA-seq analyses revealed that GLP-1/Notch signaling was downregulated, while lysosome, and PMK-1/p38 MAPK signalings were upregulated by the germline-specific inx-14 RNAi in C. elegans. Loss function of either inx-14, or glp-1 exhibited enhanced resistance to PA14 infection and upregulated lysosome and PMK-1/p38 signalings. Additionally, inx-14 knockdown by germline specific RNAi upregulated muscarinic acetylcholine receptor (mAChR) genes gar-1/gar-2/gar-3. We further revealed that acetylcholine mAChR GAR-2/GAR-3 signaling functions in the intestine and downstream of lysosome signaling but upstream of PMK-1/p38 pathway to facilitate the intestinal defense. Our findings reveal a novel role for gonadal gap junction/INX-14 in host intestinal defense against pathogens and expand our understanding the functions of reproductive system in the host intestinal defense.

2023-11-01 | GSE216879 | GEO

Influence of p38 MAPK (PMK-1) on the heat stress response of C. elegans

Project description:PMK-1 is involved in the heat stress response of C. elegans, translocates to the nucleus upon heat exposure and influences the expression of chaperone genes, proteasomal subunits and protein-biosynthesis related genes. Differential Gene expression of WT and pmk-1 deletion mutant (KU25) after 5 hours at 35Â°C

2012-11-05 | E-GEOD-41205 | biostudies-arrayexpress

Analysis of PMK-1 p38 MAPK and PMK-1(D327E) Caspase Cleavage Resistant Mutant and Effect of DAF-16 (FOXO) Mutants on Gene Regulation in C. elegans

Project description:We identified genes inversely regulated by pmk-1 null mutation and pmk-1(D327E). We also identified genes working through daf-16, working around daf-16 and working independent of daf-16

2022-07-12 | GSE192941 | GEO

Influence of p38 MAPK (PMK-1) on the heat stress response of C. elegans

2012-11-05 | GSE41205 | GEO

Analyses of CED-3 caspase and PMK-1 p38 MAPK in gene regulation in C elegans

Project description:We identified more than 300 genes inversely regulated by ced-3 and pmk-1 that enriched for epidermal stress response factors in C elegans

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Genes regulated by PMK-1 and DAF-16 in a daf-2(e1368) background.

Project description:Analysis of genes differentially expressed between daf-2(e1368) and daf-2(e1368);pmk-1(km25) and between daf-2(e1368) and daf-2(e1368);daf-16(mgDf47). These studies identified genes upregulated by wild-type PMK-1 and wild-type DAF-16. Keywords: genetic modification

2007-02-08 | GSE5801 | GEO

Gap junctions suppress electrical but not [Ca(2+)] heterogeneity in resistance arteries.

Project description:Despite stochastic variation in the molecular composition and morphology of individual smooth muscle and endothelial cells, the membrane potential along intact microvessels is remarkably uniform. This is crucial for coordinated vasomotor responses. To investigate how this electrical homogeneity arises, a virtual arteriole was developed that introduces variation in the activities of ion-transport proteins between cells. By varying the level of heterogeneity and subpopulations of gap junctions (GJs), the resulting simulations shows that GJs suppress electrical variation but can only reduce cytosolic [Ca(2+)] variation. The process of electrical smoothing, however, introduces an energetic cost due to permanent currents, one which is proportional to the level of heterogeneity. This cost is particularly large when electrochemically different endothelial-cell and smooth-muscle-cell layers are coupled. Collectively, we show that homocellular GJs in a passively open state are crucial for electrical uniformity within the given cell layer, but homogenization may be limited by biophysical or energetic constraints. Owing to the ubiquitous presence of ion transport-proteins and cell-cell heterogeneity in biological tissues, these findings generalize across most biological fields.

| S-EPMC4241449 | biostudies-literature

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