Genetic evidence for posterior specification by convergent extension in the <i>Xenopus</i> embryo

Yamada, Tsuneo; Modak, Sohan P.

doi:10.1046/j.1440-169x.1998.00002.x

Cited by 5 publications

(3 citation statements)

References 40 publications

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“…Fibroblast growth factors (FGF) play important roles in the developing embryos of various animals. In vertebrates, FGF signals are involved in embryonic growth, the establishment of mesoderm and neural tissues and the anteroposterior patterning of the trunk and tail region of the body (Slack 1994;Doniach 1995;Yamaguchi & Rossant 1995;Yamada & Modak 1998). Inhibition of FGF signaling by the dominant-negative forms of FGF receptors (FGFR) produces deficiencies in the posterior structure and results in embryos with reduced mesoderm (Amaya et al 1991;Yamaguchi et al 1994;Griffin et al 1995).…”

Section: Introductionmentioning

confidence: 99%

Role of the FGF and MEK signaling pathway in the ascidian embryo

2001

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In the ascidian embryo, a fibroblast growth factor (FGF)-like signal from presumptive endoderm blastomeres between the 32-cell and early 64-cell stages induces the formation of notochord and mesenchyme cells. However, it has not been known whether endogenous FGF signaling is involved in the process. Here it is shown that 64-cell embryos exhibit a marked increase in endogenous extracellular signal-regulated kinase (ERK/MAPK) activity. The increase in ERK activity was reduced by treatment with an FGF receptor 1 inhibitor, SU5402, and a MEK (ERK kinase/MAPKK) inhibitor, U0126. Both drugs blocked the formation of notochord and mesenchyme when embryos were treated at the 32-cell stage, but not at the 2-or 110-cell stages. The dominant-negative form of Ras also suppressed notochord and mesenchyme formation. Both inhibitors suppressed induction by exogenous basic FGF. These results suggest that the FGF signaling cascade is indeed necessary for the formation of notochord and mesenchyme cells during ascidian embryogenesis. It is also shown that FGF signaling is required for formation of the secondary notochord, secondary muscle and neural tissues, and at least ERK activity is necessary for the formation of trunk lateral cells and posterior endoderm. Therefore, FGF and MEK signaling are required for the formation of various tissues in the ascidian embryo.

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Section: Introductionmentioning

confidence: 99%

Role of the FGF and MEK signaling pathway in the ascidian embryo

2001

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“…obs., 2001). It regulates posterior specification (for reviews see Yamada 1994; Yamada & Modak 1998). We showed that both PN‐induced primitive streaks and the caudal end of the host axis express Brachyury.…”

Section: Discussionmentioning

confidence: 99%

“…Thus, PN induce mesodermalization. The suggestion that homeobox genes Xnot , Xhox3 and pintallavis are involved in caudalization (Yamada 1994; Yamada & Modak 1998) needs to be tested.…”

Section: Discussionmentioning

confidence: 99%

Post‐nodal mesoblast caudalizes the host axis and inhibits cell population growth, and induces new primitive streaks in chick embryos

et al. 2002

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One to eight post-nodal fragments (PN) or Hensen's nodes (HN) from full primitive streak stage chick embryos were transplanted onto the area pellucida or area opaca of stage 4 embryos and cultured for 20 h. Thirteen morphological and numerical parameters were affected in the host embryos and analyzed by multiple logistic regression for parametric hierarchy. In the area pellucida, both PN and HN transplants inhibited cell population growth while only PN caudalized the host axis and induced supernumerary primitive streaks expressing the mesoderm-specific gene Brachyury. In the area opaca, neither grafts influenced host axis morphogenesis, but PN inhibited the cell population growth significantly. Tracking [ 3 H]TdR labeled grafts showed that PN cells migrated towards the host axis and participated in the formation of supernumerary somites and hearts. When placed near the host axis, PN caudalized it and inhibited cell population growth.

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Ethanol exposure affects gene expression in the embryonic organizer and reduces retinoic acid levels

Yelin

Schyr

Kot

et al. 2005

Developmental Biology

110

163

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Fetal Alcohol Spectrum Disorder (FASD) is a set of developmental malformations caused by alcohol consumption during pregnancy. Fetal Alcohol Syndrome (FAS), the strongest manifestation of FASD, results in short stature, microcephally and facial dysmorphogenesis including microphthalmia. Using Xenopus embryos as a model developmental system, we show that ethanol exposure recapitulates many aspects of FAS, including a shortened rostro-caudal axis, microcephally and microphthalmia. Temporal analysis revealed that Xenopus embryos are most sensitive to ethanol exposure between late blastula and early/mid gastrula stages. This window of sensitivity overlaps with the formation and early function of the embryonic organizer, Spemann's organizer. Molecular analysis revealed that ethanol exposure of embryos induces changes in the domains and levels of organizer-specific gene expression, identifying Spemann's organizer as an early target of ethanol. Ethanol also induces a defect in convergent extension movements that delays gastrulation movements and may affect the overall length. We show that mechanistically, ethanol is antagonistic to retinol (Vitamin A) and retinal conversion to retinoic acid, and that the organizer is active in retinoic acid signaling during early gastrulation. The model suggests that FASD is induced in part by an ethanol-dependent reduction in retinoic acid levels that are necessary for the normal function of Spemann's organizer.

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Genetic evidence for posterior specification by convergent extension in the Xenopus embryo

Cited by 5 publications

References 40 publications

Role of the FGF and MEK signaling pathway in the ascidian embryo

Role of the FGF and MEK signaling pathway in the ascidian embryo

Post‐nodal mesoblast caudalizes the host axis and inhibits cell population growth, and induces new primitive streaks in chick embryos

Ethanol exposure affects gene expression in the embryonic organizer and reduces retinoic acid levels

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