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神经肽信号调节 在化感受体基因中的信息素介导的基因表达。

Neuropeptide Signaling Regulates Pheromone-Mediated Gene Expression of a Chemoreceptor Gene in .

机构信息

Department of Brain and Cognitive Sciences, DGIST, Daegu 42988, Korea.

Department of Chemistry, University of Florida, Gainesville, FL 32611, USA.

出版信息

Mol Cells. 2019 Jan 31;42(1):28-35. doi: 10.14348/molcells.2018.0380. Epub 2018 Nov 14.

Abstract

Animals need to be able to alter their developmental and behavioral programs in response to changing environmental conditions. This developmental and behavioral plasticity is mainly mediated by changes in gene expression. The knowledge of the mechanisms by which environmental signals are transduced and integrated to modulate changes in sensory gene expression is limited. Exposure to ascaroside pheromone has been reported to alter the expression of a subset of putative G protein-coupled chemosensory receptor genes in the ASI chemosensory neurons of (Kim et al., 2009; Nolan et al., 2002; Peckol et al., 1999). Here we show that ascaroside pheromone reversibly represses expression of the chemoreceptor gene in the ASI neurons. Repression of expression can be initiated only at the L1 stage, but expression is restored upon removal of ascarosides at any developmental stage. Pheromone receptors including SRBC-64/66 and SRG-36/37 are required for repression. Moreover, pheromone-mediated repression is mediated by FLP-18 neuropeptide signaling via the NPR-1 neuropeptide receptor. These results suggest that environmental signals regulate chemosensory gene expression together with internal neuropeptide signals which, in turn, modulate behavior.

摘要

动物需要能够改变其发育和行为程序,以应对不断变化的环境条件。这种发育和行为可塑性主要是通过基因表达的变化来介导的。然而,对于环境信号如何转导和整合,以调节感觉基因表达变化的机制知之甚少。已经有报道称,线虫信息素能够改变 (Kim 等人,2009;Nolan 等人,2002;Peckol 等人,1999)中 ASI 化学感觉神经元中一组假定的 G 蛋白偶联化学感觉受体基因的表达。在这里,我们显示线虫信息素可可逆地抑制 ASI 神经元中 化学受体基因的表达。 表达的抑制只能在 L1 阶段开始,但在任何发育阶段去除线虫信息素后,表达都会恢复。包括 SRBC-64/66 和 SRG-36/37 在内的信息素受体对于 表达的抑制是必需的。此外,线虫信息素介导的 表达抑制是通过 FLP-18 神经肽信号通过 NPR-1 神经肽受体来介导的。这些结果表明,环境信号与内部神经肽信号一起调节化学感觉基因表达,而神经肽信号反过来又调节行为。

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