BMP signalling in early Xenopus development

Dale, Leslie; Jones, C. Michael

doi:10.1002/(sici)1521-1878(199909)21:9<751::aid-bies6>3.0.co;2-i

Cited by 152 publications

(95 citation statements)

References 88 publications

(115 reference statements)

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“…This evidence confirms an old idea that vertebrates and arthropods share a common "bilaterian" ancestor that was inverted in one of these during evolution (see DeRobertis and Sasai, 1996;Ferguson, 1996). The conservation of mechanism goes several steps further (reviewed in Dale and Jones, 1999;Niehrs et al, 2000;Ray and Wharton, 2001). For example, BMP1 and its Drosophila counterpart, Tolloid, unlike the other BMPs, are proteases that both function to cleave and thereby inactivate the BMP/Dpp antagonists chordin/sog (Marques et al, 1997;Blader et al, 1997;Goodman et al, 1998;Wardle et al, 1999).…”

Section: Morphogens In Vivo Part Ii: Fgfs and Bmpssupporting

confidence: 79%

“…In addition to the Hedgehog morphogens and the TGF-␤-related activin and nodal proteins, there is evidence in the Xenopus blastula and gastrula for long-range action of BMP inhibitors noggin and chordin (Jones and Smith, 1998;Blitz et al, 2000). Given that there is no evidence for a gradient of BMP4 itself and that BMP4 has only a very short range of action (Jones et al, 1996), the apparently graded effects of BMP4 signaling in the embryo, thus, may be due to an oppositely directed gradient of these BMP inhibitors in vivo (see Dale and Jones, 1999).…”

Section: Establishment Of Morphogen Gradients Part I: Evidence For Dmentioning

confidence: 99%

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Morphogen gradients, positional information, and Xenopus: Interplay of theory and experiment

Green

2002

Developmental Dynamics

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The idea of morphogen gradients has long been an important one in developmental biology. Studies with amphibians and with Xenopus in particular have made significant contributions to demonstrating the existence, identity, and mechanisms of action of morphogens. Mesoderm induction and patterning by activin, nodals, bone morphogenetic proteins, and fibroblast growth factors have been analyzed thoroughly and reveal recurrent and combinatorial roles for these protein growth factor morphogens and their antagonists. The dynamics of nodal-type signaling and the intersection of VegT and ␤-catenin intracellular gradients reveal detailed steps in early long-range patterning. Interpretation of gradients requires sophisticated mechanisms for sharpening thresholds, and the activin-Xbra-Gsc system provides an example of this. The understanding of growth factor signal transduction has elucidated growth factor morphogen action and provided tools for dissecting their direct longrange action and distribution. The physical mechanisms of morphogen gradient establishment are the focus of new interest at both the experimental and theoretical level. General themes and emerging trends in morphogen gradient studies are discussed.

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Section: Morphogens In Vivo Part Ii: Fgfs and Bmpssupporting

confidence: 79%

Section: Establishment Of Morphogen Gradients Part I: Evidence For Dmentioning

confidence: 99%

Morphogen gradients, positional information, and Xenopus: Interplay of theory and experiment

Green

2002

Developmental Dynamics

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“…The alk6b homozygotes do not exhibit defects during embryogenesis, despite the importance of BMP signaling for embryonic development (38)(39)(40). This result may partly be explained by maternal expression of the wild-type alk6b allele, and partly by functional redundancy in this pathway.…”

Section: Discussionmentioning

confidence: 95%

Mutation in the type IB bone morphogenetic protein receptor alk6b impairs germ-cell differentiation and causes germ-cell tumors in zebrafish

Neumann

Chandler²,

Damoulis³

et al. 2011

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

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Germ-cell tumors (GCTs), which arise from pluripotent embryonic germ cells, exhibit a wide range of histologic differentiation states with varying clinical behaviors. Although testicular GCT is the most common cancer of young men, the genes controlling the development and differentiation of GCTs remain largely unknown. Through a forward genetic screen, we previously identified a zebrafish mutant line, tgct, which develops spontaneous GCTs consisting of undifferentiated germ cells [Neumann JC, et al. (2009) Zebrafish 6:319-327]. Using positional cloning we have identified an inactivating mutation in alk6b, a type IB bone morphogenetic protein (BMP) receptor, as the cause of the zebrafish GCT phenotype. Alk6b is expressed in spermatogonia and early oocytes, and alk6b mutant gonads display impaired BMP signal transduction, altered expression of BMP target genes, and abnormal germ-cell differentiation. We find a similar absence of BMP signaling in undifferentiated human GCTs, such as seminomas and embryonal carcinoma, but not in normal testis or in differentiated GCTs. These results indicate a germ-cell-autonomous role for BMP signal transduction in germ-cell differentiation, and highlight the importance of the BMP pathway in human GCTs.non-seminoma | SMAD | teleost | haplotype

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“…14 Differences in anterior neural induction between Xenopus and other vertebrates have been documented previously. For example, inhibiting BMP signaling by overexpressing follistatin, Noggin, or Chordin, anteriorizes Xenopus embryos; 25 however, BMP inhibition is not sufficient to induce a neural cell fate in chick or mouse embryos. 26 Similarly, overexpression of cerberus induces head formation in Xenopus embryos, but head formation is normal in mice null for Cer1.…”

Section: Discussionmentioning

confidence: 99%

Insulin-like growth factor signaling regulates zebrafish embryonic growth and development by promoting cell survival and cell cycle progression

et al. 2007

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Although much is known about the global effects of insulin-like growth factor 1 receptor (IGF1R)-mediated signaling on fetal growth and the clinical manifestations resulting from IGF/IGF1R deficiencies, we have an incomplete understanding of the cellular actions of this essential pathway during vertebrate embryogenesis. In this study, we inhibited IGF1R signaling during zebrafish embryogenesis using antisense morpholino oligonucleotides or a dominant-negative IGF1R fusion protein. IGF1R inhibition resulted in reduced embryonic growth, arrested development and increased lethality. IGF1R-deficient embryos had significant defects in the retina, inner ear, motoneurons and heart. No patterning abnormalities, however, were found in the brain or other embryonic tissues. At the cellular level, IGF1R inhibition increased caspase 3 activity and induced neuronal apoptosis. Coinjection of antiapoptotic bcl2-like mRNA attenuated the elevated apoptosis and rescued the retinal and motoneuron defects, but not the developmental arrest. Subsequent cell cycle analysis indicated an increased percentage of cells in G1 and a decreased percentage in S phase in IGF1R-deficient embryos independent of apoptosis. These results provide novel insight into the cellular basis of IGF1R function and show that IGF1R signaling does not function as an anteriorizing signal but regulates embryonic growth and development by promoting cell survival and cell cycle progression.

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BMP signalling in early Xenopus development

Cited by 152 publications

References 88 publications

Morphogen gradients, positional information, and Xenopus: Interplay of theory and experiment

Morphogen gradients, positional information, and Xenopus: Interplay of theory and experiment

Mutation in the type IB bone morphogenetic protein receptor alk6b impairs germ-cell differentiation and causes germ-cell tumors in zebrafish

Insulin-like growth factor signaling regulates zebrafish embryonic growth and development by promoting cell survival and cell cycle progression

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