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The effect of deletion of muscarinic acetylcholine receptor 4 in Math1 expressing cells in the small intestine

ABSTRACT: The effect of deletion of muscarinic acetylcholine receptor 4 in Math1 expressing cells in the small intestine

PROVIDER: PRJNA1123146 | ENA |

REPOSITORIES: ENA

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			Action	DRS
		Other
	SRR29369852_1.fastq.gz	Fastqsanger.gz
	SRR29369852_2.fastq.gz	Fastqsanger.gz
	SRR29369853_1.fastq.gz	Fastqsanger.gz
	SRR29369853_2.fastq.gz	Fastqsanger.gz

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The effect of deletion of muscarinic acetylcholine receptor 4 in Math1 expressing cells in the small intestine

Project description:The muscarinic acetylcholine receptor 4 was inducibly deleted in Math1 expressing lineages and alterations in gene expression evaluated by bulk RNA sequencing

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Molecular mechanism of muscarinic acetylcholine receptor M3 interaction with Gq

Project description:Muscarinic acetylcholine receptor M3 (M3) and its downstream effector Gq/11 are critical drug development targets given their involvement in numerous physiological processes and diseases. Although a cryo-electron microscopy study previously defined the structure of the M3-miniGq complex, the lack of information on the intracellular loop 3 (ICL3) of M3 and α-helical domain (AHD) of Gαq has made it difficult to comprehend the molecular mechanism of M3-Gq coupling fully. Here, we present the molecular mechanism underlying the dynamic interactions between the wild-type full-length M3 and heterotrimeric Gq using hydrogen-deuterium exchange mass spectrometry and NanoLuc Binary Technology-based cell systems. This study suggests potential binding interfaces between M3 and Gq in pre-assembled and fully active nucleotide-free complexes. In addition to well-known binding interfaces, we observed the interaction of long ICL3 with Gβγ. Furthermore, M3 ICL3 negatively affected M3-Gq coupling, and the Gαq AHD underwent unique conformational changes during M3-Gq coupling. Therefore, we propose a comprehensive molecular mechanism of M3-Gq coupling by analyzing previously well-defined binding interfaces and neglected regions, such as M3 ICL3 and the Gαq AHD.

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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.

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