Myosin-dependent junction remodelling controls planar cell intercalation and axis elongation

124

134

As organisms develop, their tissues can become separated into distinct cell populations through the establishment of compartment boundaries. Compartment boundaries have been discovered in a wide variety of tissues, but in many cases the molecular mechanisms that separate cells remain poorly understood. In the Drosophila wing, a stripe of Notch activation maintains the dorsal-ventral compartment boundary, through a process that depends on the actin cytoskeleton. Here, we show that the dorsal-ventral boundary exhibits a distinct accumulation of Myosin II, and that this accumulation is regulated downstream of Notch signaling. Conversely, the dorsal-ventral boundary is depleted for the Par-3 homologue Bazooka. We further show that mutations in the Myosin heavy chain subunit encoded by zipper can impair dorsal-ventral compartmentalization without affecting anterior-posterior compartmentalization. These observations identify a distinct accumulation and requirement for Myosin activity in dorsal-ventral compartmentalization, and suggest a novel mechanism in which contractile tension along an F-actin cable at the compartment boundary contributes to compartmentalization. Developmental Dynamics 235: 3051-3058, 2006.

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Localization and requirement for Myosin II at the dorsal‐ventral compartment boundary of the Drosophila wing

Major

Irvine

2006

124

134

“…Rok's primary role is to phosphorylate myosin II regulatory light chain, which leads to myosin II activation and thick filament formation. In studies using Y-27632, myosin cortical localization and myosin-dependent cell-shape changes are disrupted within a minute of drug application (Royou et al, 2002;Bertet et al, 2004;Fernandez-Gonzalez et al, 2009).…”

Section: Introductionmentioning

confidence: 99%

Assessing the critical period for Rho kinase activity during Drosophila ventral furrow formation

Krajcovic

Minden

2012

Background: Drosophila ventral furrow formation (VFF), which is the first morphogenetic event during embryo development, serves as a model for epithelial sheet folding. VFF can be subdivided into five cell shape changes: apical membrane flattening, apicobasal nuclear migration, apicobasal cell shortening, random apical constriction, and concerted apical constriction. These processes are generally believed to be driven by Rho kinase (Rok) activation of myosin II to stimulate the constriction of the apical actomyosin network. To test the role of Rok and its downstream target myosin II in VFF, timed injections of the Rok inhibitor, Y-27632, were performed. Results: Embryos injected with Y-27632 before the concerted apical constriction phase of VFF were able to execute apicobasal nuclear migration and random apical constriction, but were unable to enter the concerted apical constriction phase. Embryos injected with Y-27632 during concerted apical constriction reverted to the transition point between random apical constriction and concerted apical constriction. Finally, embryos injected with Y-27632 upon the initiation of furrow ingression were able to complete VFF. Conclusions: Together these results suggest a critical period for Rok activity and presumably myosin II activation during the initiation of the concerted apical constriction phase of VFF.

“…In fact, cells do not delaminate or migrate across the tissue but, instead, rearrange specific contacts after an ordered spatial-temporal pattern of junction remodeling. It has been proposed that axis elongation in Drosophila occurs through stereotyped cell-shape changes across a uniform field (Bertet et al, 2004). However, this model stipulates a single round of intercalation, whereas multiple rounds are required for full elongation.…”

Section: Introductionmentioning

confidence: 99%

Gain of affinity point mutation in the serotonin receptor gene 5‐HT_2Dro accelerates germband extension movements during Drosophila gastrulation

Schaerlinger

Launay

Vonesch

et al. 2007

Serotonin (5-HT) not only works as a neurotransmitter in the nervous system, but also as a morphogenetic factor during early embryogenesis. In Drosophila, a previous report showed that embryos that lack the 5-HT 2Dro receptor locus, display abnormal gastrulation movements. In this work, we screened for point mutations in the 5-HT 2Dro receptor gene. We identified one point mutation that generates a gain of serotonin affinity for the receptor and affects germband extension: 5-HT 2Dro C1644 . Embryos homozygous for this point mutation display a fourfold increase in the maximal speed of ectodermal cell movements during the rapid phase of germband extension. Homozygous 5-HT 2Dro C1644 embryos present a cuticular phenotype, including a total lack of denticle belt. Identification of this gain of function mutation shows the participation of serotonin in the regulation of the cell speed movements during the germband extension and suggests a role of serotonin in the regulation of cuticular formation during early embryogenesis. Developmental Dynamics 236:991-999, 2007.