The morphogenetic movements that shape embryos depend on the forces generated by embryo's cells and on the resistance of its tissues to these forces. Microtubules and F-actin are largely responsible for both these cellular properties but the contribution of these structural elements to morphogenesis is unclear. Now, Lance Davidson and colleagues unexpectedly report that nocodazole-induced depolymerization of microtubules stiffens the converging and extending dorsal tissues in Xenopus embryos (see ). The researchers attribute this result to the release of Xlfc – a guanine exchange factor that binds to microtubules and that regulates actomyosin contractility by activating Rho family GTPases. Consistent with this idea, drugs that reduce actomyosin contractility rescue nocodazole-induced embryonic stiffening and partly rescue the morphogenetic defects of stiffened embryos. Other experiments that combine drug treatments and Xlfc activation and knockdown indicate that microtubules have no direct role in maintaining bulk tissue stiffness in Xenopus embryos. The researchers conclude, therefore, that microtubules indirectly regulate the mechanical properties of embryonic tissues through RhoGTPase pathways.
