Pulsed actin-myosin network contractions drive apical constriction
By Adam C. Martin, M. Kaschube, E. Wieschaus. Nature, 2008
1,171 citations recorded by the source corpus.
Apical constriction facilitates epithelial sheet bending and invagination during morphogenesis. Apical constriction is conventionally thought to be driven by the continuous purse-string-like contraction of a circumferential actin and non-muscle myosin-II (myosin) belt underlying adherens junctions. However, it is unclear whether other force-generating mechanisms can drive this process. Here we show, with the use of real-time imaging and quantitative image analysis of Drosophila gastrulation, that the apical constriction of ventral furrow cells is pulsed. Repeated constrictions, which are asynchronous between neighbouring cells, are interrupted by pauses in which the constricted state of the cell apex is maintained. In contrast to the purse-string model, constriction pulses are powered by actin–myosin network contractions that occur at the medial apical cortex and pull discrete adherens junction sites inwards. The transcription factors Twist and Snail differentially regulate pulsed constriction. Expression of snail initiates actin–myosin network contractions, whereas expression of twist stabilizes the constricted state of the cell apex. Our results suggest a new model for apical constriction in which a cortical actin–myosin cytoskeleton functions as a developmentally controlled subcellular ratchet to reduce apical area incrementally.
Subfields: Cell Biology, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/f1758faa3216043b996d7936d75d187212295296
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Citations in the corpus
- Epithelial-mesenchymal transitions: insights from development (2012, background): “Twist inhibits String, a Cdc25 homolog that is essential for entry into mitosis (Grosshans and Wieschaus, 2000), and regulates apical constriction of cells via actomyosin contractility (Martin et al., 2009).”
- The ins and outs of the epithelial to mesenchymal transition in health and disease. (2011, background): “…Snail and Twist factors) are activated during the migration of neural crest in vertebrates and during gastrulation both in vertebrates and in Drosophila, although vertebrates undergo a full EMT program and the fly a partial EMT (Kolsch et al. 2007, Martin et al. 2009, Thiery et al. 2009).”
- Mechanical tugging force regulates the size of cell–cell junctions (2010, background): “Proc Natl Acad Sci USA 100(4):1484–1489.”
- Mechanical control of tissue and organ development (2010, background): “Snail generates reversible pulsed apical constrictions that are subsequently followed by a Twist-dependent collective cell constriction through the stimulation of actomyosin-based contractility via Rho/ROCK pathway activation, which leads to tissue invagination in Drosophila (Martin et al., 2009).”
- Epithelial-mesenchymal transitions in development and disease. (2009, background): “Simultaneously, Snail represses E-cadherin transcription (Oda et al., 1998) and generates the pulses of myosin contraction required for apical constriction while Twist maintains the constricted state between pulses (Martin et al., 2009).”
- Engineering microscale topographies to control the cell–substrate interface (2012, background): “embryo development and tissue morphogenesis [182,183].”