Transcription of muscle-specific actin genes in early xenopus development: Nuclear transplantation and cell dissociation

Gurdon, J. B.; Brennan, S.; Fairman, S.; Mohun, Tim

doi:10.1016/0092-8674(84)90264-2

Cited by 125 publications

(41 citation statements)

References 22 publications

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“…RT-polymerase chain reaction (PCR) analysis of stage 11.5 explants revealed that Xbrachyury (Xbra), an early mesoderm marker (Smith et al, 1991), and Zic3, a pro-neural and neural crest marker (Nakata et al, 1997), were induced by Tpr-Met expression at a level that induces ectopic tail-like structures in embryos. While a robust induction of a late mesoderm marker (muscle actin) was observed, only a small induction of a pan neural marker (NCAM) (Gurdon et al, 1984;Jacobson and Rutishauser, 1986;Kim et al, 1997) was evident ( Figure 3i). Also of interest, a posterior neural marker (Krox20) was induced by Tpr-Met, while an anterior neural marker (En2) was not.…”

Section: Tpr-met Induces Ectopic Structuresmentioning

confidence: 99%

Oncogenic Met receptor induces ectopic structures in Xenopus embryos

Ishimura

et al. 2006

Oncogene

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When aberrantly expressed or activated, the Met receptor tyrosine kinase is involved in tumor invasiveness and metastasis. In this study, we have used the Xenopus embryonic system to define the role of various Met proximal-binding partners and downstream signaling pathways in regulating an induced morphogenetic event. We show that expression of an oncogenic derivative of the Met receptor (Tpr-Met) induces ectopic morphogenetic structures during Xenopus embryogenesis. Using variant forms of Tpr-Met that are engineered to recruit a specific signaling molecule of choice, we demonstrate that the sole recruitment of either the Grb2 or the Shc adaptor protein is sufficient to induce ectopic structures and anterior reduction, while the recruitment of PI-3Kinase (PI-3K) is necessary but not sufficient for this effect. In contrast, the recruitment of PLCc can initiate the induction, but fails to maintain or elongate supernumerary structures. Finally, evidence indicates that the Ras/Raf/MAPK pathway is necessary, but not sufficient to induce these structures. This study also emphasizes the importance of examining signaling molecules in the regulatory context that is provided by receptor/effector interactions when assessing a role in cell growth and differentiation.

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Section: Tpr-met Induces Ectopic Structuresmentioning

confidence: 99%

Oncogenic Met receptor induces ectopic structures in Xenopus embryos

Ishimura

et al. 2006

Oncogene

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“…4 A and B) are probably attributable to delayed division of some cells before the normal stage of zygotic gene expression. The extinction and reactivation of genes has been described before in amphibian nuclear transplant embryos, but only in embryos that undergo normal cleavage (30)(31)(32). Mammalian experiments have demonstrated abnormal imprinted (33) and nonimprinted (34) gene expression in cloned embryos but these embryos were derived from cultured donor cells, and culturing cells could be a possible cause of aberrant gene expression (23,33).…”

Section: Activation Of Early Embryo Genesmentioning

confidence: 99%

From intestine to muscle: Nuclear reprogramming through defective cloned embryos

Byrne

Simonsson

Gurdon

2002

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

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Nuclear transplantation is one of the very few ways by which the genetic content and capacity for nuclear reprogramming can be assessed in individual cells of differentiated somatic tissues. No more than 6% of the cells of differentiated tissues have thus far been shown to have nuclei that can be reprogrammed to elicit the formation of unrelated cell types. In Amphibia, about 25% of such nuclear transfers form morphologically abnormal partial blastulae that die within 24 h. We have investigated the genetic content and capacity for reprogramming of those nuclei that generate partial blastulae, using as donors the intestinal epithelium cells of feeding Xenopus larvae. We have analyzed single nuclear transplant embryos obtained directly from intestinal tissue, thereby avoiding any genetic or epigenetic changes that might accumulate during cell culture. The expression of the intestine-specific gene intestinal fatty acid binding protein is extinguished by at least 10 4 times, within a few hours of nuclear transplantation. At the same time several genes that are normally expressed only in early embryos are very strongly activated in nuclear transplant embryos, but to an unregulated extent. Remarkably, cells from intestine-derived partial blastulae, when grafted to normal host embryos, contribute to several host tissues and participate in the normal 100-fold increase in axial muscle over several months. Thus, cells of defective cloned embryos unable to survive for more than 1 day can be reprogrammed to participate in new directions of differentiation and to maintain indefinite growth, despite the abnormal expression of early genes.

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“…Animals were housed and fed as described previously (Gurdon et al, 1984). Eggs were fertilised in vitro and the embryos were chemically dejellied with 2% (wt/vol) cysteine-HCl, pH 7.8/7.9, then maintained in 1× MBS (Modified Barth's solution pH 7.6 (Gurdon and Wickens, 1983) until microinjection.…”

Section: Embryos and Microinjectionsmentioning

confidence: 99%

Control of embryonicXenopusmorphogenesis by a Ral-GDS/Xral branch of the Ras signalling pathway

Lebreton

Boissel

Moreau

2003

Journal of Cell Science

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Ras proteins mediate biological responses through various effectors and play a key role in relaying the Fibroblast Growth Factor (FGF) mesoderm induction signal during embryogenesis of the frog, Xenopus laevis. One Ras effector pathway involves the activation of the small G protein Ral. In the present study, we have investigated the role of key components in the Ral branch of FGF and Ras signalling during early Xenopus development. Treatment of animal caps with bFGF, which converts prospective ectoderm to mesoderm, activates Xral. The Ras mutant 12V37G, which can bind to Ral-GDS but not Raf, also activates Xral as well as causing developmental defects and cortical F-actin disassembly. A similar phenotype is induced by Ral-GDS itself. FGF-induced expression of several signature mesodermal genes, by contrast, is independent of Xral signalling. This and other data suggest that the RalB branch of Ras and FGF signalling regulates the actin cytoskeleton and morphogenesis in a transcriptionally independent manner. We also find Xral to be specifically activated in the marginal zone of Xenopus embryos, and find that disruption of the Ral pathway in this region prevents closure of the blastopore during gastrulation. We conclude that Ral signalling is autonomously required by mesodermal cells to effect essential morphogenetic changes during Xenopus gastrulation.

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Transcription of muscle-specific actin genes in early xenopus development: Nuclear transplantation and cell dissociation

Cited by 125 publications

References 22 publications

Oncogenic Met receptor induces ectopic structures in Xenopus embryos

Oncogenic Met receptor induces ectopic structures in Xenopus embryos

From intestine to muscle: Nuclear reprogramming through defective cloned embryos

Control of embryonicXenopusmorphogenesis by a Ral-GDS/Xral branch of the Ras signalling pathway

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