Abstract
Contractile actomyosin networks generate forces that drive tissue morphogenesis. Actomyosin contractility is controlled primarily by reversible phosphorylation of the myosin-II regulatory light chain through the action of myosin kinases and phosphatases. While the role of myosin light-chain kinase in regulating contractility during morphogenesis has been largely characterized, there is surprisingly little information on myosin light-chain phosphatase (MLCP) function in this context. Here, we use live imaging of Drosophila follicle cells combined with mathematical modelling to demonstrate that the MLCP subunit flapwing (flw) is a key regulator of basal myosin oscillations and cell contractions underlying egg chamber elongation. Flw expression decreases specifically on the basal side of follicle cells at the onset of contraction and flw controls the initiation and periodicity of basal actomyosin oscillations. Contrary to previous reports, basal F-actin pulsates similarly to myosin. Finally, we propose a quantitative model in which periodic basal actomyosin oscillations arise in a cell-autonomous fashion from intrinsic properties of motor assemblies.
Highlights
Contractile actomyosin networks generate forces that drive tissue morphogenesis
Myosin light-chain phosphatase (MLCP), a heterotrimer consisting of a Ser/Thr phosphatase catalytic subunit (PP1c), a myosin phosphatase targeting subunit (MYPT1/2) and a 20-kDa small subunit, performs the opposite role, myosin inactivation via MRLC dephosphorylation[5]
One well-studied example of basal cell contraction essential for tissue morphogenesis is that of the follicle cells (FCs) during egg formation in the adult Drosophila ovary
Summary
Contractile actomyosin networks generate forces that drive tissue morphogenesis. Actomyosin contractility is controlled primarily by reversible phosphorylation of the myosin-II regulatory light chain through the action of myosin kinases and phosphatases. Actomyosin-driven cell contractility is indispensable during morphogenesis for the acquisition of the threedimensional shape of tissues and organs[1] It relies on forces generated by the contraction of an actin filament network through the activity of the motor protein non-muscle myosin-II (Myo-II)[2]. We identify flapwing (flw), which codes for one of the four PP1c subunits that exist in Drosophila, as a key regulator of basal contractile activity in FCs. We show that at S9, concomitant with the onset of basal contraction, Flw expression decreases on the basal side of FCs. In addition, we find that flw is required for the initiation and periodicity of basal myosin oscillations. In contrast to previous observations[8], we demonstrate that basal F-actin undergoes periodic pulsations to myosin Based on these observations and using in silico modelling, we propose that cell-autonomous basal actomyosin oscillations governing egg chamber elongation arise from the intrinsic properties of motor assemblies
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