Regulation of <i>hlh-2</i> transcription during specification of the anchor cell of the <i>C. elegans</i> hermaphrodite gonad
The anchor cell (AC) of the Caenorhabditis elegans hermaphrodite somatic gonad primordium is a signaling nexus that regulates uterine and vulval development. As the somatic gonad primordium is forming, four cells, two α and two β cells, are born with the potential to be the AC. This potential becomes restricted to the α cells, which undergo the LIN-12/Notch-mediated AC/VU decision to resolve which α cell will become the AC. The transcription factor HLH-2, the sole E/Daughterless protein ortholog in C. elegans, is critical for this process, and dynamic regulation of hlh-2 transcription contributes to the robust specification of a single AC. The hlh-2prox regulatory element mediates the dynamic pattern of hlh-2 transcription: the initial expression in the parents of the α and β cells, which is briefly sustained in the α and β cells after they are born; its subsequent restriction to the α cells during the AC/VU decision; and its continued expression in the AC. In this study, we identify the cis-acting sequences within hlh-2prox and transcription factors required for the initial expression of hlh-2 in the α and β cells and their parents, demonstrate that the Wnt/β-catenin Asymmetry Pathway (WβA) regulates restriction of hlh-2 transcription to the α cells, and show that the maintenance of hlh-2 transcription in α cells requires distinct elements and the chromatin factor LSY-12. This analysis extends our understanding of regulatory mechanisms that operate during a precise and robust Notch-mediated lateral specification paradigm.
Authors
- Iva Greenwald (ORCID: https://orcid.org/0000-0001-7180-3706)
- J. Kim (ORCID: https://orcid.org/0000-0003-0304-3738)
Institutions
- Columbia University (US)
Publication Details
- Journal
- G3 Genes Genomes Genetics
- Published
- 2025-12-02
- DOI
- https://doi.org/10.1093/g3journal/jkaf288
- Primary Topic
- Genetics, Aging, and Longevity in Model Organisms
- Type
- article
- Field-Weighted Citation Impact
- 0.00
Funders
- National Institutes of Health
- National Institute of General Medical Sciences