TY  - GEN
T1  - unc-42 regulates the expression of ASH terminal fate markers
AU  - Wood, Jordan F
AU  - Ferkey, Denise M
DO  - 10.17912/micropub.biology.000114
UR  - http://beta.micropublication.org/journals/biology/micropub-biology-000114/
AB  - The genes encoding transcription factors that initiate the terminal differentiation programs within individual neurons have been termed “terminal selectors” (Hobert 2008).  They are considered master regulators of neuronal identity because they integrate upstream lineage inputs to ultimately drive (directly and/or indirectly) the expression of all terminal differentiation features of a neuron (Hobert 2008; Bertrand and Hobert 2010). The paired-like homeodomain transcription factor UNC-42 has been proposed to function as the terminal selector in the developmental specification of the ASH polymodal nociceptors in C. elegans (Baran et al. 1999). Consistent with the role of a terminal selector, unc-42(e419) loss-of-function mutants were shown to lack the expression of the putative chemoreceptor genes sra-6 and srb-6 specifically in the ASHs, while, for example, srb-6 expression in the ADL and ADF sensory neurons was unaffected (Baran et al. 1999). unc-42(e419) mutants also lack ASH expression of several other terminal identity markers: three Gα encoding genes (gpa-11, gpa-13 and gpa-15), the neuropeptide encoded by flp-21, and the eat-4 vesicular glutamate transporter (Serrano-Saiz et al. 2013).  Furthermore, loss of UNC-42 function disrupted behavioral responses to high osmolarity and nose touch (Baran et al. 1999), which are both detected primarily by the ASHs (Bargmann et al. 1990; Kaplan and Horvitz 1993).  However, the severity of the nose touch defect was likely due to developmental defects in both the ASH sensory neurons as well as some downstream interneurons, where altered glutamate receptor expression accompanies loss of UNC-42 (Baran et al. 1999; Brockie et al. 2001).
PY  - 2019
JO  - microPublication Biology
ER  -