The CMK-1 CaMKI and the TAX-4 cyclic nucleotide-gated channel regulate thermosensory neuron gene expression and function in C-elegans

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.