TY  - GEN
T1  - Deletion of a putative HDA-1 binding site in the hlh-2 promoter eliminates expression in C. elegans dorsal uterine cells
AU  - Medwig-Kinney, Taylor N
AU  - Palmisano, Nicholas J
AU  - Matus, David Q
DO  - 10.17912/micropub.biology.000449
UR  - http://beta.micropublication.org/journals/biology/micropub-biology-000449/
AB  - During C. elegans development, two cells, Z1 and Z4, give rise to the entire somatic gonad, including populations of dorsal uterine (DU) and ventral uterine (VU) cells, as well as the postmitotic anchor cell (AC), which invades the underlying basement membrane during uterine-vulval morphogenesis (Kimble & Hirsh, 1979; Sherwood & Sternberg, 2003). The helix-loop-helix transcription factor hlh-2 (E/Daughterless) is expressed in these three cell types, among others, and is particularly enriched in the AC following post-transcriptional down-regulation of HLH-2 in the VU through dimerization-driven degradation (Karp & Greenwald, 2003; Sallee & Greenwald, 2015). At the L2 stage, HLH-2 regulates the Notch signaling event that specifies AC and VU fates, with its initial onset predicting the lineage ultimately giving rise to the presumptive VU (Karp & Greenwald, 2004; Attner et al., 2019). Following AC/VU specification, HLH-2 functions to regulate cell cycle arrest and invasion of the AC (Medwig-Kinney et al., 2020; Schindler & Sherwood, 2011). We and others have shown that HLH-2 does so by regulating expression of the nuclear hormone receptor and transcription factor NHR-67 (Tailless/TLX/NR2E1), and likely cell-cycle independent, pro-invasive targets as well (Bodofsky et al., 2018; Medwig-Kinney et al., 2020).
PY  - 2021
JO  - microPublication Biology
ER  -