RESUMEN
During epithelial contraction, cells generate forces to constrict their surface and, concurrently, fine-tune the length of their adherens junctions to ensure force transmission. While many studies have focused on understanding force generation, little is known on how junctional length is controlled. Here, we show that, during amnioserosa contraction in Drosophila dorsal closure, adherens junctions reduce their length in coordination with the shrinkage of apical cell area, maintaining a nearly constant junctional straightness. We reveal that junctional straightness and integrity depend on the endocytic machinery and on the mechanosensitive activity of the actomyosin cytoskeleton. On one hand, upon junctional stretch and decrease in E-cadherin density, actomyosin relocalizes from the medial area to the junctions, thus maintaining junctional integrity. On the other hand, when junctions have excess material and ruffles, junction removal is enhanced, and high junctional straightness and tension are restored. These two mechanisms control junctional length and integrity during morphogenesis.
Asunto(s)
Citoesqueleto de Actina/metabolismo , Actomiosina/metabolismo , Uniones Adherentes/fisiología , Morfogénesis/fisiología , Animales , Cadherinas/metabolismo , Proteínas de Drosophila/metabolismo , Drosophila melanogaster/citología , Endocitosis/fisiologíaRESUMEN
Dorsal closure, a late-embryogenesis process, consists in the sealing of an epidermal gap on the dorsal side of the Drosophila embryo. Because of its similarities with wound healing and neural tube closure in humans, it has been extensively studied in the last twenty years. The process requires the coordination of several force generating mechanisms, that together will zip shut the epidermis. Recent works have provided a precise description of the cellular behavior at the origin of these forces and proposed quantitative models of the process. In this review, we will describe the different forces acting in dorsal closure. We will present our current knowledge on the mechanisms generating and regulating these forces and report on the different quantitative mathematical models proposed so far.
Asunto(s)
Drosophila melanogaster/embriología , Desarrollo Embrionario/genética , Epidermis/embriología , Regulación del Desarrollo de la Expresión Génica , Modelos Estadísticos , Actinas/genética , Actinas/metabolismo , Animales , Fenómenos Biomecánicos , Tipificación del Cuerpo/genética , Proteínas Relacionadas con las Cadherinas/genética , Proteínas Relacionadas con las Cadherinas/metabolismo , Proteínas de Drosophila/genética , Proteínas de Drosophila/metabolismo , Drosophila melanogaster/genética , Drosophila melanogaster/metabolismo , Embrión no Mamífero , Células Epidérmicas , Epidermis/metabolismo , Genes Reporteros , Proteínas Fluorescentes Verdes/genética , Proteínas Fluorescentes Verdes/metabolismo , Transducción de SeñalRESUMEN
Biological tissues must generate forces to shape organs and achieve proper development. Such forces often result from the contraction of an apical acto-myosin meshwork. Here we describe an alternative mechanism for tissue contraction, based on individual cell volume change. We show that during Drosophila dorsal closure (DC), a wound healing-related process, the contraction of the amnioserosa (AS) is associated with a major reduction of the volume of its cells, triggered by caspase activation at the onset of the apoptotic program of AS cells. Cell volume decrease results in a contractile force that promotes tissue shrinkage. Estimating mechanical tensions with laser dissection and using 3D biophysical modeling, we show that the cell volume decrease acts together with the contraction of the actin cable surrounding the tissue to govern DC kinetics. Our study identifies a mechanism by which tissues generate forces and movements by modulating individual cell volume during development.