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@article{Ferrando-Marco:2026:10.1242/dev.205658,
author = {Ferrando-Marco, M and Lin, S and Del, Valle BG and Hintze, M and Narunsky, L and Huang, J and Edwards, S and Barkoulas, M},
doi = {10.1242/dev.205658},
journal = {Development},
title = {HDAC1/2-mediated repression of Wnt receptor expression orients asymmetric division polarity in C. elegans.},
url = {http://dx.doi.org/10.1242/dev.205658},
year = {2026}
}
TY - JOUR
AB - Asymmetric cell division generates distinct daughter cells essential for tissue development, yet the mechanisms orienting division polarity within tissues remain incompletely understood. Here, we uncover a role for chromatin-mediated transcriptional repression in controlling polarity orientation during asymmetric division of C. elegans epidermal stem cells, known as the seam cells. Tissue-specific loss of the class I histone deacetylase hda-1, homologous to mammalian HDAC1/2, causes polarity reversals and reduces molecular asymmetry between daughter cells. Using Targeted DamID, we identify the Wnt receptors lin-17/Frizzled and cam-1/Ror as key targets. Single-molecule FISH reveals opposing expression gradients along the body axis, with cam-1 enriched anteriorly and lin-17 posteriorly. In hda-1 mutants, both receptors are upregulated and differences between seam cells are flattened. Overexpression of either receptor alone is sufficient to reproduce the polarity reversals, while co-overexpression produces additive effects. The polarity phenotype is independent of the canonical NuRD and SIN3 complexes, suggesting that HDA-1 acts through an alternative mechanism. These findings link histone deacetylase activity to Wnt receptor expression and suggest that graded receptor expression may provide cues that orient asymmetric division polarity.
AU - Ferrando-Marco,M
AU - Lin,S
AU - Del,Valle BG
AU - Hintze,M
AU - Narunsky,L
AU - Huang,J
AU - Edwards,S
AU - Barkoulas,M
DO - 10.1242/dev.205658
PY - 2026///
TI - HDAC1/2-mediated repression of Wnt receptor expression orients asymmetric division polarity in C. elegans.
T2 - Development
UR - http://dx.doi.org/10.1242/dev.205658
UR - https://www.ncbi.nlm.nih.gov/pubmed/42544752
ER -
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