期刊
CURRENT BIOLOGY
卷 14, 期 1, 页码 62-68出版社
CELL PRESS
DOI: 10.1016/j.cub.2003.12.030
关键词
-
资金
- NCRR NIH HHS [S10 RR16780] Funding Source: Medline
- NIGMS NIH HHS [F32 GM20048] Funding Source: Medline
- NINDS NIH HHS [T32 NS07292, P01 NS44232] Funding Source: Medline
The cultivation temperature (T-c) modulates the thermosensory responses exhibited by C. elegans on thermal gradients [1-5]. The AFD sensory neurons are essential for thermosensory behaviors [2], but the molecular mechanisms by which temperature is sensed and the memory of the T-c is encoded are unknown. Here, we show that the CMK-1 Ca2+/calmodulin-dependent protein kinase I (CaMKI) and the TAX-4 cyclic nucleotide-gated channel regulate gene expression, morphology, and functions of the AFD thermosensory neurons. Mutations in cmk-1 and tax-4 result in temperature-dependent defects in AFD-specific gene expression, and TAX-4 functions are required during larval stages to maintain gene expression in the adult. CMK-1 and TAX-4 act cell autonomously to regulate AFD-mediated thermosensory behaviors. The molecular requirements for CMK-1 activity in the AFD neurons appear to be distinct from those previously described [6, 7]. We propose that the activation of distinct programs of AFD-specific gene expression at different temperatures by CMK-1 and TAX-4 enables C. elegans to sense and/or encode a memory for the T-c.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据