Transcription factors are important cellular determinants of specification and development. We describe the transcript and expression pattern analyses of the Caenorhabditis elegans homeobox gene C02F12.10. The predicted exon-intron structure of C02F12.10 would encode a small homeodomain protein of 152 amino acids but had no transcript data support. Sequence directed PCR amplification on a cDNA library, generated from mixed staged C. elegans, confirmed the predicted single transcript. GFP expression driven by the promoter of this transcript and a recombineered-fosmid encoded N-terminal translational GFP fusion for C02F12.10 showed specific expression in the single interneuron DVC, in the dorso-rectal ganglion, from late embryo to adult and, as yet unidentified, uterus cells in young adults only. In contrast, a C-terminal translational GFP fusion, expressed from a recombineered fosmid, displayed a broader distribution, including DVC, uterus and other nerve cells in the head and tail region. The inconsistent expression patterns of N- and C-terminal fusions indicate that either there are alternative transcripts of C02F12.10 present at very low abundance in the cDNA library or there are extra cis-acting elements, located in the intron/coding sequence of C02F12.10, whose action is disrupted by GFP insertion near the promoter. The possibility of an alternative C02F12.10 isoform, initiating from an internal ATG in the second exon, is being tested. Loss-of-function C02F12.10 deletion mutants are viable and fertile and do not show any obvious locomotion defects. We are further characterizing possible DVC identity defects in the C02F12.10 deletion mutants. Another two homeodomain transcription factors CEH-14 and MBR-1, expressed broadly in C. elegans nerve cells including DVC, were found to act upstream and downstream of C02F12.10 respectively. Expression of
mbr-1::gfp in DVC was eliminated by the C02F12.10 deletion and expression of C02F12.10::gfp in DVC was greatly attenuated or abolished in the
ceh-14 (
ch3) deletion mutant. The major synaptic outputs of DVC are to the main command interneurons AVA and AVB, which drives backward and forward locomotion respectively. Using the DVC-specific C02F12.10 promoter we specifically targeted the light-gated cation channel channelrhodopsin-2 (ChR2) to DVC without interfering with other neurons in the circuit. While light stimulation of body wall muscles, the pharyngeal MC motor neurons and the ventral cord VB motor neurons, via ChR2 driven by the promoters from
myo-3,
ceh-19b, and
ceh-12 respectively, displayed specific and robust behavioural responses, we have not so far observed any specific response upon light stimulation of DVC.