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Comments on Kagoshima, Hiroshi et al. (2009) International Worm Meeting "Systematic analyses of AFD-specific enhancers in C. elegans." (0)
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Kagoshima, Hiroshi, Kajiwara, Junko, & Kohara, Yuji (2009). Systematic analyses of AFD-specific enhancers in C. elegans presented in International Worm Meeting. Unpublished information; cite only with author permission.
How can transcription factors control gene expression in the right place and at the right time? To investigate the mechanism of the cell-specific transcriptional regulation, we chose AFD thermosensory neuron for our target cell. We performed systematic deletion analyses of nine AFD-specific genes using promoter::GFP reporters, and narrowed down the DNA sequences required for AFD expression to relatively small regions (from 50 bp to 600 bp). Among these AFD-specific promoters, gcy-8 and gcy-18 promoters are particularly interesting, because these genes may have arisen from gene duplication and most probably they were controlled by the same regulatory mechanism. This notion is supported by following data: their expression were similar in spatial pattern (exclusively expressed in AFD) [Inada et al. 2006] and in temporal control (initiated at pre-comma stage), and were downregulated by either of the mutants, ttx-1 or ceh-14 (both of which encode homeobox transcription factors expressed in AFD) [Satterlee et al. 2001 and this work]. Moreover, the expression of gcy-8 and gcy-18 are completely abolished in ttx-1; ceh-14 double mutant background. We also showed that forced expression of both transcription factors in AWB chemosensory neuron could induce ectopic expression of gcy-8 and gcy-18 in AWB. These results suggest that ttx-1 and ceh-14 genes play pivotal roles in gcy-8 and gcy-18 expression. We found these promoters shared common 7-8 bp DNA motifs, which are conserved in five Caenorhabditis species (C. elegans, C. briggsae, C. brenneri, C. remanei and C. japonica). We are currently analyzing the promoters of gcy-8 and gcy-18 orthologs of the Caenorhabditis species in C. elegans. Further analysis will be reported at the meeting.