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
m
ating).
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-19
M
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.