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First published online 30 May 2007
doi: 10.1242/dev.005074

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The RhoGAP RGA-2 and LET-502/ROCK achieve a balance of actomyosin-dependent forces in C. elegans epidermis to control morphogenesis

Marie Diogon^1,*, Frédéric Wissler^1,, Sophie Quintin^1,, Yasuko Nagamatsu¹, Satis Sookhareea¹, Frédéric Landmann¹, Harald Hutter^2,, Nicolas Vitale³ and Michel Labouesse^1,

¹ IGBMC, CNRS/INSERM/ULP, 1 rue Laurent Fries, BP.10142, 67400 Illkirch, France.
² MPI for Medical Research, Jahnstr. 29, 69120 Heidelberg, Germany.
³ Institut des Neurosciences Cellulaires et Intégratives, UMR 7168 CNRS, 67084 Strasbourg, France.

Author for correspondence (e-mail: lmichel{at}igbmc.u-strasbg.fr)

Accepted 11 April 2007

Embryonic morphogenesis involves the coordinate behaviour of multiple cells and requires the accurate balance of forces acting within different cells through the application of appropriate brakes and throttles. In C. elegans, embryonic elongation is driven by Rho-binding kinase (ROCK) and actomyosin contraction in the epidermis. We identify an evolutionary conserved, actin microfilament-associated RhoGAP (RGA-2) that behaves as a negative regulator of LET-502/ROCK. The small GTPase RHO-1 is the preferred target of RGA-2 in vitro, and acts between RGA-2 and LET-502 in vivo. Two observations show that RGA-2 acts in dorsal and ventral epidermal cells to moderate actomyosin tension during the first half of elongation. First, time-lapse microscopy shows that loss of RGA-2 induces localised circumferentially oriented pulling on junctional complexes in dorsal and ventral epidermal cells. Second, specific expression of RGA-2 in dorsal/ventral, but not lateral, cells rescues the embryonic lethality of rga-2 mutants. We propose that actomyosin-generated tension must be moderated in two out of the three sets of epidermal cells surrounding the C. elegans embryo to achieve morphogenesis.

Key words: ARHGAP20, C. elegans, Rho-kinase, RhoGAP, Epithelial, Morphogenesis

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