Control of
            <i>Drosophila</i>
            Gastrulation by Apical Localization of Adherens Junctions and RhoGEF2

Kölsch, Verena; Seher, Thomas C.; Fernandez-Ballester, Gregorio J.; Serrano, Luís; Leptin, Maria

doi:10.1126/science.1134833

Cited by 306 publications

(357 citation statements)

References 21 publications

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“…In embryos that are mutant for fog, T48, or dia (Diaphanous, a formin), myosin II fails to accumulate (Dawes-Hoang et al, 2005; Developmental Dynamics Kolsch et al, 2007;DeMaman et al, 2008). In fog and T48 mutants, Rho-GEF2, which activates Rok, is not recruited efficiently to the apical surface.…”

Section: Discussion Apical Myosin II Localization During Vff Is Depenmentioning

confidence: 99%

“…Briefly, Toll signaling induces the expression of transcriptional regulators Twist (Twi) and Snail (Sna). Twi activates the expression of folded gastrulation (Fog) and T48 (Costa et al, 1994;Kolsch et al, 2007). Fog is a secreted factor that binds to an as-yet-unidentified receptor to activate the Ga protein, Concertina (Cta) at the apical surface of ventral cells.…”

Section: Developmental Dynamicsmentioning

confidence: 99%

“…Cta mediates the activation and release of RhoGEF2 from EB1 on microtubules (Rogers et al, 2004). T48 also recruits RhoGEF2 to the apical membrane through PDZ interactions (Kolsch et al, 2007). RhoGEF2 then locally activates Rho and Rok to constrict an actomyosin network, driving apical constriction (Rogers et al, 2004).…”

Section: Developmental Dynamicsmentioning

confidence: 99%

“…Myosin II is thought to be required for the apical constriction of VFF; however, embryos that are mutant for twi, fog, or T48, still experience some random apical constriction (Oda and Tsukita, 2001;Kolsch et al, 2007;Martin et al, 2009). These proteins are all implicated in recruiting and activating myosin II apically (Twi drives the expression of Fog and T48).…”

Section: Rho Kinase Inhibitor Does Not Block Random Apical Constrictionmentioning

confidence: 99%

“…These proteins are all implicated in recruiting and activating myosin II apically (Twi drives the expression of Fog and T48). However, in vivo studies have shown that myosin II is only weakly present during the early constriction events, and high levels are only accumulated after apical flattening (Kolsch et al, 2007;Witzberger et al, 2008). Therefore, it was important to ascertain whether myosin II is required for random apical constriction.…”

Section: Rho Kinase Inhibitor Does Not Block Random Apical Constrictionmentioning

confidence: 99%

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

Krajcovic

Minden

2012

Developmental Dynamics

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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.

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Section: Discussion Apical Myosin II Localization During Vff Is Depenmentioning

confidence: 99%

Section: Developmental Dynamicsmentioning

confidence: 99%

Section: Developmental Dynamicsmentioning

confidence: 99%

Section: Rho Kinase Inhibitor Does Not Block Random Apical Constrictionmentioning

confidence: 99%

Section: Rho Kinase Inhibitor Does Not Block Random Apical Constrictionmentioning

confidence: 99%

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

Krajcovic

Minden

2012

Developmental Dynamics

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Engineering a Cell Home for Stem Cell Homing and Accommodation

Yin

et al. 2017

Adv. Biosys.

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Distilling complexity to advance regenerative medicine from laboratory animals to humans, in situ regeneration will continue to evolve using biomaterial strategies to drive endogenous cells within the human body for therapeutic purposes; this approach avoids the need for delivering ex vivo‐expanded cellular materials. Ensuring the recruitment of a significant number of reparative cells from an endogenous source to the site of interest is the first step toward achieving success. Subsequently, making the “cell home” cell‐friendly by recapitulating the natural extracellular matrix (ECM) in terms of its chemistry, structure, dynamics, and function, and targeting specific aspects of the native stem cell niche (e.g., cell–ECM and cell–cell interactions) to program and steer the fates of those recruited stem cells play equally crucial roles in yielding a therapeutically regenerative solution. This review addresses the key aspects of material‐guided cell homing and the engineering of novel biomaterials with desirable ECM composition, surface topography, biochemistry, and mechanical properties that can present both biochemical and physical cues required for in situ tissue regeneration. This growing body of knowledge will likely become a design basis for the development of regenerative biomaterials for, but not limited to, future in situ tissue engineering and regeneration.

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Polarity and cell fate specification in the control of Caenorhabditis elegans gastrulation

Rohrschneider

Nance

2009

Developmental Dynamics

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Gastrulation is a time during development when cells destined to produce internal tissues and organs move from the surface of the embryo into the interior. It is critical that the cell movements of gastrulation be precisely controlled, and coordinated with cell specification, in order for the embryo to develop normally. Caenorhabditis elegans gastrulation is relatively simple, can be observed easily in the transparent embryo, and can be manipulated genetically to uncover important regulatory mechanisms. Many of these cellular and molecular mechanisms, including cell shape, cytoskeletal, and cell cycle changes, appear to be conserved from flies to vertebrates. Here we review gastrulation in C. elegans, with an emphasis on recent data linking contact-induced cell polarity, PAR proteins, and cell fate specification to gastrulation control.

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Control of Drosophila Gastrulation by Apical Localization of Adherens Junctions and RhoGEF2

Cited by 306 publications

References 21 publications

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

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

Engineering a Cell Home for Stem Cell Homing and Accommodation

Polarity and cell fate specification in the control of Caenorhabditis elegans gastrulation

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