Neuronal Acetylcholine Couples Gonadal Gap Junction/Notch Signaling Axis to Gut Defense
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ABSTRACT:
PROVIDER: PRJNA896101 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR22104200_1.fastq.gz | Fastqsanger.gz | |||
| SRR22104200_2.fastq.gz | Fastqsanger.gz | |||
| SRR22104201_1.fastq.gz | Fastqsanger.gz | |||
| SRR22104201_2.fastq.gz | Fastqsanger.gz | |||
| SRR22104202_1.fastq.gz | Fastqsanger.gz |
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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
Project description:Gap junctions and purinergic P2 receptors (P2Rs) can be regarded as belonging to a common functional unit, given that they are involved in the transmission of calcium signals between cells. We have previously shown that deletion of the Gja1 gene alters expression levels of numerous genes encoding proteins with diverse functions, including purinergic, P2Rs, and have found that genes synergistically or antagonistically expressed in wildtype tissues are more prone to be similarly or oppositely regulated in Cx43-nulls. We have now explored the use of coordination analysis of gene expression as a strategy to identify interlinked genes encoding functionally related proteins and used pull-downs to evaluate their interlinkage. Our findings indicate that, in brain and in cultured astrocytes, several of these co-expressed genes encode proteins that are components of P2R signal transduction pathways and/or directly interact with these receptors, including the gap junction protein connexin43 (Cx43) and connexin45 (Cx45), as well as pannexins. It is proposed that coordination analysis of gene expression may provide a novel unbiased strategy for the identification of proteins belonging to supramolecular complexes. Keywords: genetic modification
2007-06-20 | GSE8105 | GEO
Project description:Co-IP Experiment Bait: Cx43-Flag Cell line: Hela Related Publication: Gap Junction protein Connexin-43 is a direct transcriptional regulator of N-cadherin in vivo, Maria Kotini, Elias Barriga, Jonathan Leslie, Marc Gentzel, Verena Rauschenberger, Alexandra Schambony, and Roberto Mayor
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Project description:Disruption of the mouse gene encoding the gap junction subunit alpha3 connexin 46 (Cx46) results in the formation of lens cataracts. The timing of the onset of this lens opacity is affected by the genetic background, i.e. the mouse strain. To elucidate the mechanism by which cataracts form in the 129Sv/Jae strain earlier than in the C57BL/6J strain, global gene expression was quantitated in the lenses of these strains. Lens cDNAs were analyzed by hybridization to DNA microarrays and with real time-PCR. Theories are proposed based on the observed higher level of expression of the stress-response genes in the C57BL/6J strain and variations in the expression levels of genes involved in protein synthesis, metabolism, catabolism and cell proliferation. How these variations in gene expression might affect the response of lens fiber cells to the increased calcium, caused by lack of alpha3Cx46, is considered. The possibility that the proteins coded by the strain-variable genes might influence the cataract-associated proteolysis of gamma-crystallin is also addressed. Keywords: Lens, cataract, microarray, connexin 46, gene knock out
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Project description:How a tissue returns to homeostasis following injury remains enigmatic. Here, we show that elevated Ca2+ dynamics among enterocytes (ECs) mediated by nAchRs (nicotinic Acetylcholine (Ach) Receptor) in the adult Drosophila midgut, are essential for the epithelium to return to homeostasis after injury. This bioelectric signal is controlled by 1) changes in EC-responsiveness to Ach; 2) enteric neuro-EC interactions; and 3) epithelial gap junctions. Our findings demonstrate how a bioelectric signal during regeneration, initiated by local neuro-epithelial communication and propagated by gap junctions, is coupling the epithelium into a unified response that promotes return to homeostasis.
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Project description:Regulation of membrane receptors involves management of endocytosis. At the neuromuscular junction, the synapse between skeletal muscle and motoneuron, proper density of the major receptor, the acetylcholine receptor, is of utmost importance for sustaining life in context of mobility. Recent work has revealed innervation of NMJs by sympathetic neurons and destruction of them had morphological and functional consequences, suggesting influence on endocytosis. To investigate the pathways and proteins that are relevant for acetylcholine receptor turnover and affected by sympathetic signaling, proteomes of mouse hindlimb muscles from sympathectomized and saline-treated control muscles were compared. Using proteomic, Western blot, and immunofluorescence analysis in chemically sympathectomized mouse hindlimb muscles, the cause of these consequences were aimed to analyzed. This revealed extensive regulation of the proteome by the sympathetic nervous system and a possible regulatory function of the endo/lysosomal and autophagic pathway by sympathetic neuronal input. This finding might provide a new explanation to the observed benefit of sympathicomimetic treatment in several congenital myasthenic syndromes.
2021-03-01 | PXD021601 | Pride
Project description:Metastatic progression in bone involves crosstalk between tumor cells and osteoblasts, osteoclasts, and osteocytes. Renal cell carcinoma bone metastases (RCCBM) are predominantly osteolytic and often treatment resistant. We previously reported that inhibition of osteoblast differentiation by BIGH3 (transforming growth factor-beta-induced protein ig-h3) secreted by colonizing 786-O RCC cells promotes tumor progression in bone. Here we report that BIGH3 induces osteocyte apoptosis in both human specimens and mice and inhibits gap junction (GJ) protein Cx43 expression and function, disrupting bone homeostasis. As proof-of-concept, lysosomal inhibitors, such as hydroxychloroquine (HCQ) and NH4Cl, reversed BIGH3-mediated GJ dysfunction in vitro; and inhibited tumor growth and reversed Bo-786 RCC-induced osteolysis in vivo. HCQ in combination with CBZ, but not alone, reversed the RCCBM-mediated decreases in bone mineral density and osteoblast numbers, and decreased osteocyte apoptosis and osteoclast recruitment. These BIGH3 associated impacts on the bone microenvironment comprise a noncanonical mechanism of metastasis progression.
2024-09-18 | GSE244453 | GEO
Project description:Disruption of the mouse gene encoding the gap junction subunit alpha3 connexin 46 (Cx46) results in the formation of lens cataracts. The timing of the onset of this lens opacity is affected by the genetic background, i.e. the mouse strain. To elucidate the mechanism by which cataracts form in the 129Sv/Jae strain earlier than in the C57BL/6J strain, global gene expression was quantitated in the lenses of these strains. Lens cDNAs were analyzed by hybridization to DNA microarrays and with real time-PCR. Theories are proposed based on the observed higher level of expression of the stress-response genes in the C57BL/6J strain and variations in the expression levels of genes involved in protein synthesis, metabolism, catabolism and cell proliferation. How these variations in gene expression might affect the response of lens fiber cells to the increased calcium, caused by lack of alpha3Cx46, is considered. The possibility that the proteins coded by the strain-variable genes might influence the cataract-associated proteolysis of gamma-crystallin is also addressed. Experiment Overall Design: To determine differences in transcript expression between the lenses of two mouse wild type strains (129 SvJae and C57BL/6J), as well as between alpha3Cx46 KO and wild-type mice. The former comparison may lead to identification of potential candidate(s) genes that prevent (or promote) cataract formation, whereas the latter comparison may provide insights into the mechanism by which cataract formation occurs in the alpha3Cx46 KO mice. Total 8 samples were used ( two separate samples for each of the following 4 types of mice: 129SvJae wild type, 129SvJae alpha3Cx46 KO, C57BL/6J wild type and C57BL/6J alpha3Cx46 KO)
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