In Situ Activation Pattern of
            <i>Drosophila</i>
            EGF Receptor Pathway During Development

Gabay, Limor; Seger, Rony; Shilo, Ben‐Zion

doi:10.1126/science.277.5329.1103

Cited by 367 publications

(285 citation statements)

References 34 publications

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“…In addition, the genetic link between RhoA and Mek/Erk pathway can be further supported by their reminiscent expression domain during embryonic development, for example, rhoA (Zhu et al, 2006) and erk (Krens et al, 2006) are both highly expressed in forebrain, midbrainhindbrain boundary, hindbrain, eyes and tail region during zebrafish embryonic development. And, the similar expression profile of RhoA and the phosphor-Erk are very conserved from fly to vertebrate (Gabay et al, 1997;Corson et al, 2003), suggesting that functions of these proteins in embryogenesis could be genetically linked during evolution.…”

Section: Discussionmentioning

confidence: 99%

RhoA prevents apoptosis during zebrafish embryogenesis through activation of Mek/Erk pathway

et al. 2007

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RhoA small GTPase, as a key regulator for actin cytoskeletal rearrangement, plays pivotal roles during morphogenesis, cytokinesis, phagocytosis and cell migration, but little is known about its signaling mechanism that controls cell survival in vivo. Using zebrafish as a model, we show that non-overlapping antisense morpholinos that block either translation or splicing of rhoA lead to extensive apoptosis during embryogenesis, resulting in overall reduction of body size and body length. These defects are associated with reduced activation of growth-promoting Erk and decreased expression of anti-apoptotic bcl-2. Moreover, ectopic expression of rhoA, Mek or BCL-2 mRNA rescues such phenotypes. Consistently, combined suppression of RhoA and Mek/Erk or Bcl-2 pathways by sub-optimal dose of rhoA morpholino and pharmacological inhibitors for either Mek (U0126) or Bcl-2 (HA 14-1) can induce developmental abnormalities and enhanced apoptosis, similar to those caused by effective RhoA knockdown. Furthermore, U0126 abrogates the rescue by RhoA and MEK but not BCL-2. In contrast, HA 14-1 effectively abolishes all functional rescues by RhoA, MEK or BCL-2, supporting that RhoA prevents apoptosis by activation of Mek/Erk pathway and requiring Bcl-2. These findings reveal an important genetic and functional relationship between RhoA with Mek/Erk and Bcl-2 for cell survival control during embryogenesis.

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Section: Discussionmentioning

confidence: 99%

RhoA prevents apoptosis during zebrafish embryogenesis through activation of Mek/Erk pathway

et al. 2007

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“…A leading role is attributed to the MAPK/ERK pathway, in insect (Gabay et al, 1997) and vertebrate development (Northrop et al, 1995;Umbhauer et al, 1995). Another signaling pathway, that leads through phosphatidyl-inositol 3-kinase (PI 3-kinase) and Akt/PKB, is also induced by the same receptors.…”

Section: Introductionmentioning

confidence: 99%

Fibroblast growth factor (FGF) signaling through PI 3-kinase and Akt/PKB is required for embryoid body differentiation

et al. 2000

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The role of FGF signaling in early epithelial di erentiation was investigated in ES (embryonic stem) cell derived embryoid bodies. A dominant negative ®broblast growth factor receptor (FGFR) mutation was created by stably introducing into ES cells an Fgfr2 cDNA, truncated in its enzymatic domains. These cells failed to di erentiate into cystic embryoid bodies. No epithelial di erentiation and cavitation morphogenesis could be observed, in the mutant, although its rate of cell proliferation remained unchanged. This phenotype was associated with a signi®cant decrease in the activation of Akt/PKB and PLCg-1, as compared to the wild type, while the activation of MAPK/Erk was less a ected. Requirement for PI 3-kinase signaling in embryoid body di erentiation was demonstrated by speci®c inhibitors. Akt/PKB activation was abrogated by wortmannin in short-term experiments. In long-term cultures Ly294002 inhibited the di erentiation of ES cells into embryoid bodies. Our data demonstrate that for early epithelial di erentiation FGF signaling is required through the PI 3-kinase-Akt/ PKB pathway.

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“…vein encodes a secreted EGF signaling molecule (18,19), whereas rho encodes a membrane protease that releases the Spitz EGF ligand from ventral regions of the neurogenic ectoderm (20,21). These EGF signals activate MAP kinase in both ventral and lateral regions of the neurogenic ectoderm (22). In principle, ind can be activated in both regions by the combination of low levels of the Dorsal gradient and EGF signaling, but expression is kept off in the ventral neurogenic ectoderm by Vnd, a sequencespecific transcriptional repressor that is activated by intermediate levels of Dorsal ( Fig.…”

Section: Cell-cell Interactions Produce Additional Dorsal Gradient Rementioning

confidence: 99%

How the Dorsal gradient works: Insights from postgenome technologies

Hong

Hendrix

Papatsenko

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

123

133

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Gradients of extracellular signaling molecules and transcription factors are used in a variety of developmental processes, including the patterning of the Drosophila embryo, the establishment of diverse neuronal cell types in the vertebrate neural tube, and the anterior-posterior patterning of vertebrate limbs. Here, we discuss how a gradient of the maternal transcription factor Dorsal produces complex patterns of gene expression across the dorsal-ventral (DV) axis of the early Drosophila embryo. The identification of 60 -70 Dorsal target genes, along with the characterization of Ϸ35 associated regulatory DNAs, suggests that there are at least six different regulatory codes driving diverse DV expression profiles.Drosophila ͉ regulatory code ͉ embryo ͉ morphogen T he dorsal-ventral (DV) patterning of the early Drosophila embryo is controlled by a sequence-specific transcription factor, Dorsal, which is related to mammalian NF-B (1-3). Differential activation of the Toll receptor leads to the formation of a broad Dorsal nuclear gradient, with peak levels present in ventral regions and progressively lower levels in lateral and dorsal regions (Fig.

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In Situ Activation Pattern of Drosophila EGF Receptor Pathway During Development

Cited by 367 publications

References 34 publications

RhoA prevents apoptosis during zebrafish embryogenesis through activation of Mek/Erk pathway

RhoA prevents apoptosis during zebrafish embryogenesis through activation of Mek/Erk pathway

Fibroblast growth factor (FGF) signaling through PI 3-kinase and Akt/PKB is required for embryoid body differentiation

How the Dorsal gradient works: Insights from postgenome technologies

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