2005
DOI: 10.1242/dev.02056
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Rho1 regulatesDrosophilaadherens junctions independently of p120ctn

Abstract: preferentially accumulates basally or basolaterally in several tissues, but does not preferentially accumulate in AJs. Further, Rho1 localization is not obviously altered by loss of p120 or by reduction of core AJ proteins. Genetic and cell biological tests suggest that p120 is not a major dose-sensitive regulator of Rho1. However, Rho1 itself appears to be a regulator of AJs. Loss of Rho1 results in ectopic accumulation of cytoplasmic DE-cadherin, but ectopic cadherin does not accumulate with its partner Arma… Show more

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Cited by 49 publications
(47 citation statements)
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References 55 publications
(72 reference statements)
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“…These cells assemble an actin-myosin cable at their dorsal-most edge (Edwards et al, 1997;Jacinto et al, 2002a;Kaltschmidt et al, 2002;Kiehart et al, 2000) that seeds cellular protrusions, filopodia and lamellipodia, which play adhesive and segment-matching roles in the late stages of DC (Jacinto et al, 2000;Liu et al, 2008;Millard and Martin, 2008). A number of studies have implicated interactions between the cytoskeleton and cell-adhesion systems in the development and coordination of these movements (Bloor and Kiehart, 2002;Fox et al, 2005;Franke et al, 2005;Gorfinkiel and Martínez Arias, 2007;Grevengoed et al, 2001;Magie et al, 2002;Murray et al, 2006;Takahashi et al, 2005). Furthermore, laser ablation of small groups of cells in the AS or the epidermis have revealed some of the forces involved in DC.…”
Section: Introductionmentioning
confidence: 99%
“…These cells assemble an actin-myosin cable at their dorsal-most edge (Edwards et al, 1997;Jacinto et al, 2002a;Kaltschmidt et al, 2002;Kiehart et al, 2000) that seeds cellular protrusions, filopodia and lamellipodia, which play adhesive and segment-matching roles in the late stages of DC (Jacinto et al, 2000;Liu et al, 2008;Millard and Martin, 2008). A number of studies have implicated interactions between the cytoskeleton and cell-adhesion systems in the development and coordination of these movements (Bloor and Kiehart, 2002;Fox et al, 2005;Franke et al, 2005;Gorfinkiel and Martínez Arias, 2007;Grevengoed et al, 2001;Magie et al, 2002;Murray et al, 2006;Takahashi et al, 2005). Furthermore, laser ablation of small groups of cells in the AS or the epidermis have revealed some of the forces involved in DC.…”
Section: Introductionmentioning
confidence: 99%
“…Several studies have hinted at the importance of AJs and their regulation during DC (Bloor and Kiehart, 2002;Fox et al, 2005;Grevengoed et al, 2001;Magie et al, 2002;McEwen et al, 2000;Murray et al, 2006;Takahashi et al, 2005). For example, defects associated with genetic interactions between shotgun (shg), the gene encoding E-cadherin in Drosophila, and actin regulators such as the small GTPase Rho (Fox et al, 2005) and the non-receptor tyrosine kinases Src (Takahashi et al, 2005) or Abl (Grevengoed et al, 2001), suggest that some aspect of the AJs is crucial for DC.…”
Section: Introductionmentioning
confidence: 99%
“…For example, defects associated with genetic interactions between shotgun (shg), the gene encoding E-cadherin in Drosophila, and actin regulators such as the small GTPase Rho (Fox et al, 2005) and the non-receptor tyrosine kinases Src (Takahashi et al, 2005) or Abl (Grevengoed et al, 2001), suggest that some aspect of the AJs is crucial for DC. However, although some shg mutations that reach the DC stages (Tepass et al, 1996;Uemura et al, 1996), there has not been a full study of the role of AJs in this epithelial sheet movement.…”
Section: Introductionmentioning
confidence: 99%
“…The stablisation of cells within epithelia could explain other p120-catenin mutant phenotypes, such as defects in retinal patterning and rates of cell movement during dorsal closure (Fox et al, 2005;Larson et al, 2008). Combined loss of p120-catenin-binding sites and endocytic motifs from vertebrate cadherins reduced cell migration upon VEGF induction (Nanes et al, 2012) and disrupted morphogenetic movements in Xenopus embryos (Ciesiolka et al, 2004), suggesting that the function of p120-catenin in cell rearrangements is conserved between Drosophila and vertebrates.…”
Section: Two Pathways For E-cad Endocytosismentioning
confidence: 99%
“…Nonetheless, loss of p120-catenin results in developmental defects in Drosophila, including slowed morphogenetic movements during dorsal closure (Fox et al, 2005) and retinal patterning defects (Larson et al, 2008).…”
Section: Introductionmentioning
confidence: 99%