Koga Makoto, Ohshima Yasumi
Department of Biology, Faculty of Sciences, Kyushu University Graduate School, 6-10-1 Hakozaki, Higashi-Ku, Fukuoka 812-8581, Japan.
J Mol Biol. 2004 Feb 20;336(3):579-87. doi: 10.1016/j.jmb.2003.12.037.
Chemotaxis to water-soluble chemicals such as sodium ion is an important behavior of Caenorhabditis elegans for seeking food, and ASE chemosensory neurons have a major role in this behavior. We isolated mutants defective in chemotaxis to sodium acetate. We show here that among them ks86 had a mutation in the ceh-36 gene. ceh-36 :: gfp reporter constructs were expressed in ASE and AWC neurons. In a mutant of the che-1 gene, which encodes another transcription factor and is required for specification of ASE neurons, expression of the ceh-36 :: gfp reporter in ASE is lost. This indicates that the ceh-36 gene functions downstream of the che-1 gene in ASE. In the ceh-36(ks86) mutant, expression of the tax-2 gene encoding a cyclic nucleotide-gated channel was reduced in ASE and AWC. This affords an explanation for defects of the ceh-36 mutant in the chemotaxis mediated by ASE and AWC. When a ceh-36 cDNA was expressed in an adult ceh-36 mutant by a heat shock promoter, chemotaxis to sodium acetate was recovered. These results suggest that ceh-36 is required for functions, and not for development, of ASE.
向水溶性化学物质（如钠离子）趋化是秀丽隐杆线虫寻找食物的重要行为，而ASE化学感受神经元在这一行为中起主要作用。我们分离出了对醋酸钠趋化有缺陷的突变体。我们在此表明，其中ks86在ceh-36基因中存在突变。ceh-36::gfp报告基因构建体在ASE和AWC神经元中表达。在che-1基因的突变体中，che-1基因编码另一种转录因子，是ASE神经元特化所必需的，ceh-36::gfp报告基因在ASE中的表达丧失。这表明ceh-36基因在ASE中在che-1基因的下游发挥作用。在ceh-36(ks86)突变体中，编码环核苷酸门控通道的tax-2基因在ASE和AWC中的表达降低。这为ceh-36突变体在由ASE和AWC介导的趋化中的缺陷提供了解释。当通过热休克启动子在成年ceh-36突变体中表达ceh-36 cDNA时，对醋酸钠的趋化得以恢复。这些结果表明，ceh-36是ASE功能所必需的，而不是其发育所必需的。
