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http://purl.uniprot.org/citations/18299395http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/18299395http://www.w3.org/2000/01/rdf-schema#comment"Posterior body wall muscle contraction (pBoc) in the nematode Caenorhabditis elegans occurs rhythmically every 45-50 s and mediates defecation. pBoc is controlled by inositol-1,4,5-trisphosphate (IP3)-dependent Ca2+ oscillations in the intestine. The intestinal epithelium can be studied by patch clamp electrophysiology, Ca2+ imaging, genome-wide reverse genetic analysis, forward genetics, and molecular biology and thus provides a powerful model to develop an integrated systems level understanding of a nonexcitable cell oscillatory Ca2+ signaling pathway. Intestinal cells express an outwardly rectifying Ca2+ (ORCa) current with biophysical properties resembling those of TRPM channels. Two TRPM homologues, GON-2 and GTL-1, are expressed in the intestine. Using deletion and severe loss-of-function alleles of the gtl-1 and gon-2 genes, we demonstrate here that GON-2 and GTL-1 are both required for maintaining rhythmic pBoc and intestinal Ca2+ oscillations. Loss of GTL-l and GON-2 function inhibits I(ORCa) approximately 70% and approximately 90%, respectively. I(ORCa) is undetectable in gon-2;gtl-1 double mutant cells. These results demonstrate that (a) both gon-2 and gtl-1 are required for ORCa channel function, and (b) GON-2 and GTL-1 can function independently as ion channels, but that their functions in mediating I(ORCa) are interdependent. I(ORCa), I(GON-2), and I(GTL-1) have nearly identical biophysical properties. Importantly, all three channels are at least 60-fold more permeable to Ca2+ than Na+. Epistasis analysis suggests that GON-2 and GTL-1 function in the IP3 signaling pathway to regulate intestinal Ca2+ oscillations. We postulate that GON-2 and GTL-1 form heteromeric ORCa channels that mediate selective Ca2+ influx and function to regulate IP3 receptor activity and possibly to refill ER Ca2+ stores."xsd:string
http://purl.uniprot.org/citations/18299395http://purl.org/dc/terms/identifier"doi:10.1085/jgp.200709914"xsd:string
http://purl.uniprot.org/citations/18299395http://purl.uniprot.org/core/author"Yan X."xsd:string
http://purl.uniprot.org/citations/18299395http://purl.uniprot.org/core/author"Xing J."xsd:string
http://purl.uniprot.org/citations/18299395http://purl.uniprot.org/core/author"Estevez A."xsd:string
http://purl.uniprot.org/citations/18299395http://purl.uniprot.org/core/author"Strange K."xsd:string
http://purl.uniprot.org/citations/18299395http://purl.uniprot.org/core/date"2008"xsd:gYear
http://purl.uniprot.org/citations/18299395http://purl.uniprot.org/core/name"J Gen Physiol"xsd:string
http://purl.uniprot.org/citations/18299395http://purl.uniprot.org/core/pages"245-255"xsd:string
http://purl.uniprot.org/citations/18299395http://purl.uniprot.org/core/title"Highly Ca2+-selective TRPM channels regulate IP3-dependent oscillatory Ca2+ signaling in the C. elegans intestine."xsd:string
http://purl.uniprot.org/citations/18299395http://purl.uniprot.org/core/volume"131"xsd:string
http://purl.uniprot.org/citations/18299395http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/18299395
http://purl.uniprot.org/citations/18299395http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/18299395
http://purl.uniprot.org/uniprot/Q93971#attribution-ECF7788619BFD1ABBB9A04072DDE7A76http://purl.uniprot.org/core/sourcehttp://purl.uniprot.org/citations/18299395
http://purl.uniprot.org/uniprot/G5ECM4#attribution-ECF7788619BFD1ABBB9A04072DDE7A76http://purl.uniprot.org/core/sourcehttp://purl.uniprot.org/citations/18299395
http://purl.uniprot.org/uniprot/G5EE91#attribution-ECF7788619BFD1ABBB9A04072DDE7A76http://purl.uniprot.org/core/sourcehttp://purl.uniprot.org/citations/18299395
http://purl.uniprot.org/uniprot/A5JYU8#attribution-ECF7788619BFD1ABBB9A04072DDE7A76http://purl.uniprot.org/core/sourcehttp://purl.uniprot.org/citations/18299395
http://purl.uniprot.org/uniprot/G5EGP7#attribution-ECF7788619BFD1ABBB9A04072DDE7A76http://purl.uniprot.org/core/sourcehttp://purl.uniprot.org/citations/18299395
http://purl.uniprot.org/uniprot/G5EGJ6#attribution-ECF7788619BFD1ABBB9A04072DDE7A76http://purl.uniprot.org/core/sourcehttp://purl.uniprot.org/citations/18299395
http://purl.uniprot.org/uniprot/#_A0A0K3AUL3-mappedCitation-18299395http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/18299395
http://purl.uniprot.org/uniprot/#_A0A0K3AUL7-mappedCitation-18299395http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/18299395
http://purl.uniprot.org/uniprot/#_A0A0K3AUM3-mappedCitation-18299395http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/18299395
http://purl.uniprot.org/uniprot/#_A0A0K3AUN1-mappedCitation-18299395http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/18299395
http://purl.uniprot.org/uniprot/#_A0A0K3AV83-mappedCitation-18299395http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/18299395