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Description
The vertebrate inner ear is a conserved sensory organ for balance. Its morphogenesis follows a two‑phase program: (i) expansion of the otic vesicle—a closed epithelial monolayer enclosing a fluid‑filled lumen—and (ii) a topological transition from a closed vesicle to the toroidal structure of the semicircular canals. Although this two-phase process is broadly conserved, previous studies \cite{mosaliganti, munjal} have reported divergence in molecular mechanisms and tissue mechanics between zebrafish and mouse during phase (ii). This raises two questions: how do distinct mechanisms yield a common morphology, and how did such divergence evolve? To address these questions, we focus on phase (i), the otic vesicle expansion phase in zebrafish and mouse, combining pharmacological perturbations with mathematical modeling. We find that zebrafish vesicles expand primarily through fluid influx into the lumen, whereas mouse vesicles expand through coupled fluid influx and mechanosensitive tissue growth. In zebrafish, limited tissue growth reflects restricted cell growth rather than reduced proliferation. Extending our analysis to 12 vertebrate species sampled broadly across the phylogeny, we identify two distinct vesicle‑expansion modes and corresponding cell‑growth programs, exemplified by zebrafish and mouse. We propose that divergence in these morphogenetic processes reflects the adaptive evolution of developmental duration, accompanied by shifts in cell‑growth programs.
Bibliography
@article{mosaliganti,
title = {Size control of the inner ear via hydraulic feedback},
volume = {8},
copyright = {http://creativecommons.org/licenses/by/4.0/},
issn = {2050-084X},
url = {https://elifesciences.org/articles/39596},
doi = {10.7554/eLife.39596},
abstract = {Animals make organs of precise size, shape, and symmetry but how developing embryos do this is largely unknown. Here, we combine quantitative imaging, physical theory, and physiological measurement of hydrostatic pressure and fluid transport in zebrafish to study size control of the developing inner ear. We find that fluid accumulation creates hydrostatic pressure in the lumen leading to stress in the epithelium and expansion of the otic vesicle. Pressure, in turn, inhibits fluid transport into the lumen. This negative feedback loop between pressure and transport allows the otic vesicle to change growth rate to control natural or experimentally-induced size variation. Spatiotemporal patterning of contractility modulates pressure-driven strain for regional tissue thinning. Our work connects molecular-driven mechanisms, such as osmotic pressure driven strain and actomyosin tension, to the regulation of tissue morphogenesis via hydraulic feedback to ensure robust control of organ size.
Editorial note: This article has been through an editorial process in which the authors decide how to respond to the issues raised during peer review. The Reviewing Editor's assessment is that all the issues have been addressed ({\textless}xref ref-type="decision-letter" rid="SA1"{\textgreater}see decision letter{\textless}/xref{\textgreater}).},
language = {en},
urldate = {2026-03-14},
journal = {eLife},
author = {Mosaliganti, Kishore R and Swinburne, Ian A and Chan, Chon U and Obholzer, Nikolaus D and Green, Amelia A and Tanksale, Shreyas and Mahadevan, L and Megason, Sean G},
month = oct,
year = {2019},
pages = {e39596},
}
@article{munjal,
title = {Extracellular hyaluronate pressure shaped by cellular tethers drives tissue morphogenesis},
volume = {184},
issn = {00928674},
url = {https://linkinghub.elsevier.com/retrieve/pii/S0092867421013738},
doi = {10.1016/j.cell.2021.11.025},
language = {en},
number = {26},
urldate = {2026-03-14},
journal = {Cell},
author = {Munjal, Akankshi and Hannezo, Edouard and Tsai, Tony Y.-C. and Mitchison, Timothy J. and Megason, Sean G.},
month = dec,
year = {2021},
pages = {6313--6325.e18},
}
