The C elegans transcription factor DMD-10 is an ortholog of the human DBRTB, a Doublesex/MAB-3(DM)-related transcription factor. Young adult
dmd-10 (
gk1131) loss-of-function mutant C. elegans exhibit selective defects in sensorimotor behaviors (Durbeck et al. 2021). They are less responsive to nose-touch mechanosensory stimulation and high osmolarity, both of which are transduced by a pair of ASH sensory neurons (Kaplan and Horvitz 1993; Bargmann 2006; Lindsay et al. 2011)
dmd-10 mutants also show an approximately 50% decrease in their behavioral response to direct, optogenetic activation of channelrhodopsin-2 expressed under the control of promoters whose expression patterns overlap only in ASH (Ezcurra et al. 2011; Durbeck et al. 2021). Considering the known effects of other DM domain-containing proteins on neuronal development (Tresser et al. 2010; Yoshizawa et al. 2011; Saulnier et al. 2013), one potential explanation for this could be that one of the two ASH neurons does not develop properly or survive in adult
dmd-10 mutant animals.