Key result
Extracellular cues including physical contact, asymmetric contact size, and Wnt signaling generate distinct cortical actomyosin flows that orient cell division axes in C. elegans and mouse embryos.
This study identifies a microtubule-independent, mechanosensitive actomyosin flow mechanism that orients cell division axes during early embryonic development.
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Reveals tunable actomyosin-based division orientation in animals; leaves open relevance to cardiac morphogenesis or regeneration.
Summary Cell division axes during animal development are arranged in diverse orientations, but the molecular mechanisms underlying this diversity remain unclear. By focusing on oriented divisions that are independent of known microtubule/dynein pathways, we show here that the non-muscle myosin II motor is an extrinsically tunable force generator that orients cell division axes through cortical actomyosin flows. We identified three extracellular cues that generate different actomyosin flows. A single contact site locally inhibited myosin activity in a mechanosensitive manner to generate local flow asymmetry, while size asymmetry of two contact sites and Wnt signaling both polarized myosin activity and actomyosin flow, with the latter overriding mechanosensitive effects. These intracellular actomyosin flow anisotropies specify distinct division axes to establish the geometries of not only Caenorhabditis elegans 4-, 6-, and 7-cell stage but also mouse 4-cell stage embryos. Tunable actomyosin flows together with microtubule/dynein pathways may specify diverse division axes across species.
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A 2017 study studied Embryonic development. Extracellular cues (physical contact, asymmetric contact size, Wnt signaling) vs. Absence of cues / symmetric contacts was evaluated on Cell division axis orientation. Extracellular cues including physical contact, asymmetric contact size, and Wnt signaling generate distinct cortical actomyosin flows that orient cell division axes in C. elegans and mouse embryos.
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