Actomyosin contractility in olfactory placode neurons opens the skin epithelium to form the zebrafish nostril
- Baraban, M., Gordillo Pi, C., Bonnet, I., Gilles, J.F., Lejeune, C., Cabrera, M., Tep, F., Breau, M.A.
- Developmental Cell 58(5): 361-375.e5 (Journal)
- Registered Authors
- Baraban, Marion, Breau, Marie
- actomyosin, epithelial hole, epithelial morphogenesis, mechanical interactions, nostril, olfactory placode neurons, orifice, skin, skin epithelium, zebrafish
- MeSH Terms
- Olfactory Mucosa
- 36841243 Full text @ Dev. Cell
Baraban, M., Gordillo Pi, C., Bonnet, I., Gilles, J.F., Lejeune, C., Cabrera, M., Tep, F., Breau, M.A. (2023) Actomyosin contractility in olfactory placode neurons opens the skin epithelium to form the zebrafish nostril. Developmental Cell. 58(5):361-375.e5.
Despite their barrier function, epithelia can locally lose their integrity to create physiological openings during morphogenesis. The mechanisms driving the formation of these epithelial breaks are only starting to be investigated. Here, we study the formation of the zebrafish nostril (the olfactory orifice), which opens in the skin epithelium to expose the olfactory neurons to external odorant cues. Combining live imaging, drug treatments, laser ablation, and tissue-specific functional perturbations, we characterize a mechanical interplay between olfactory placode neurons and the skin, which plays a crucial role in the formation of the orifice: the neurons pull on the overlying skin cells in an actomyosin-dependent manner which, in combination with a local reorganization of the skin epithelium, triggers the opening of the orifice. This work identifies an original mechanism to break an epithelial sheet, in which an adjacent group of cells mechanically assists the epithelium to induce its local rupture.
Genes / Markers
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Engineered Foreign Genes