fax-1 encodes a nuclear receptor that is the ortholog of PNR in mammals and functions in specifying neuronal identity during development.
fax-1 is expressed in a limited number of interneurons, including AVA, AVE, and AVK. The
daf-2 insulin receptor is the key mediator of insulin signaling in which downstream activation of
daf-16/FOXO-like transcription factor is implicated in increased longevity and dauer arrest. Arrest assays of
daf-2(
e1370);
fax-1 double mutants reveal quiescent arrest at hatching. This novel peri-hatching arrest phenotype is analogous to sleep, as it can be reversed with flashes of aversive blue light. These animals are rescued by downstream mutations in
daf-16 and
daf-18/PTEN, but not components of the TGF-? pathway, confirming that insulin and neuronal signaling control quiescent arrest. Interneuron AVK contributes to arousal and expresses
fax-1, which makes it a candidate as a key mediator of peri-hatching arrest. If we selectively express
fax-1 in a subset of neurons in
daf-2(
e1370);
fax-1 double mutants, we can determine in which interneurons
fax-1 expression is responsible for peri-hatching arrest. We are performing cell specific rescue assays with transgenic double mutant animals with extrachromosomal arrays that drive FAX-1 expression under the control of neuron-specific promoters.
glr-2,
npr-1,
glr-5::
fax-1::gfp fusions reveal that broad expression of FAX-1 in AVA, AVE, AVK, SIB, and RIC interneurons rescues double mutant animals from quiescence. However, animals are not rescued when FAX-1 is selectively expressed in AVA and AVE. These data suggest that AVK may be a key interneuron mediator that regulates quiescence at hatching.