Affiliation:
1. Department of Genetics, Rutgers, The State University of New Jersey, Piscataway, New Jersey 08854 and
2. Department of Biology, Massachusetts Institute Of Technology, Cambridge, Massachusetts 02139
Abstract
Abstract
In animals, RFX transcription factors govern ciliogenesis by binding to an X-box motif in the promoters of ciliogenic genes. In Caenorhabditis elegans, the sole RFX transcription factor (TF) daf-19 null mutant lacks all sensory cilia, fails to express many ciliogenic genes, and is defective in many sensory behaviors, including male mating. The daf-19c isoform is expressed in all ciliated sensory neurons and is necessary and sufficient for activating X-box containing ciliogenesis genes. Here, we describe the daf-19(n4132) mutant that is defective in expression of the sensory polycystic kidney disease (PKD) gene battery and male mating behavior, without affecting expression of ciliogenic genes or ciliogenesis. daf-19(n4132) disrupts expression of a new isoform, daf-19m (for function in male mating). daf-19m is expressed in male-specific PKD and core IL2 neurons via internal promoters and remote enhancer elements located in introns of the daf-19 genomic locus. daf-19m genetically programs the sensory functions of a subset of ciliated neurons, independent of daf-19c. In the male-specific HOB neuron, DAF-19M acts downstream of the zinc finger TF EGL-46, indicating that a TF cascade controls the PKD gene battery in this cell-type specific context. We conclude that the RFX TF DAF-19 regulates ciliogenesis via X-box containing ciliogenic genes and controls ciliary specialization by regulating non-X-box containing sensory genes. This study reveals a more extensive role for RFX TFs in generating fully functional cilia.
Publisher
Oxford University Press (OUP)