smad2 and smad3 Are Required for Mesendoderm Induction by Transforming Growth Factor-β/Nodal Signals in Zebrafish

Jia, Shaofeng; Ren, Zhen; Li, Xiang; Zheng, Ying; Meng, Anming

doi:10.1074/jbc.m707578200

Cited by 55 publications

(60 citation statements)

References 49 publications

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“…Smad2 has also been suggested to be required for mesendoderm induction in zebrafish [37]. Here, we found that Smad2 plays an essential role in expression of several mesendodermal lineage markers (e.g., Gsc, Lhx1 and Sox17).…”

Section: Discussionmentioning

confidence: 52%

Smad2 mediates Activin/Nodal signaling in mesendoderm differentiation of mouse embryonic stem cells

et al. 2010

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Although Activin/Nodal signaling regulates pluripotency of human embryonic stem (ES) cells, how this signaling acts in mouse ES cells remains largely unclear. To investigate this, we confirmed that mouse ES cells possess active Smad2-mediated Activin/Nodal signaling and found that Smad2-mediated Activin/Nodal signaling is dispensable for self-renewal maintenance but is required for proper differentiation toward the mesendoderm lineage. To gain insights into the underlying mechanisms, Smad2-associated genes were identified by genome-wide chromatin immunoprecipitation-chip analysis. The results showed that there is a transcriptional correlation between Smad2 binding and Activin/Nodal signaling modulation, and that the development-related genes were enriched among the Smad2-bound targets. We further identified Tapbp as a key player in mesendoderm differentiation of mouse ES cells acting downstream of the Activin/Nodal-Smad2 pathway. Taken together, our findings suggest that Smad2-mediated Activin/Nodal signaling orchestrates mesendoderm lineage commitment of mouse ES cells through direct modulation of corresponding developmental regulator expression.

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Section: Discussionmentioning

confidence: 52%

Smad2 mediates Activin/Nodal signaling in mesendoderm differentiation of mouse embryonic stem cells

et al. 2010

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“…This unexpected finding may have resulted from the presence of maternal Ror2 proteins (42,43). To expand our study, the dominantnegative form of zebrafish Ror2, Ror2-TM, was used to inhibit the function of wild-type Ror2 (25).…”

Section: Discussionmentioning

confidence: 99%

Ror2 Receptor Mediates Wnt11 Ligand Signaling and Affects Convergence and Extension Movements in Zebrafish

Bai

Tan

Zhang

et al. 2014

Journal of Biological Chemistry

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Background:The impact of receptor-tyrosine kinase superfamily members on zebrafish embryonic development is not well understood. Results: Zebrafish dominant-negative ror2 mRNA and ror2 mRNA expression induced incomplete eye separation in zebrafish embryos. Conclusion: Ror2 mediates Wnt11 signaling and regulates gastrulation convergence and extension movements in zebrafish. Significance: These results provide novel insights into convergence and extension movements in vertebrate gastrulation.

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“…However, they often share similar functions, playing redundant roles in ovarian granulosa cells , in zebrafish mesoderm induction (Jia et al, 2008) and in other cellular contexts (Bernard, 2004). Moreover, when introduced into the Smad2 locus, Smad3 can rescue the Smad2-deletion phenotype in developing mouse embryos (Dunn et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

Smad2 and Smad3 cooperate and antagonize simultaneously in vertebrate neurogenesis

Míguez

Gil-Guiñón

Pons

et al. 2013

Journal of Cell Science

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SummaryThe transforming growth factor beta (TGF-b) pathway plays key roles in development and cancer. TGF-b signaling converges on the Smad2 and Smad3 effectors, which can either cooperate or antagonize to regulate their transcriptional targets. Here we performed in vivo and in silico experiments to study how such cooperativity and antagonism might function during neurogenesis. In vivo electroporation experiments in the chick embryo neural tube show that Smad2 and Smad3 cooperate to promote neurogenesis, as well as the transcription of Smad3-specific targets. Knockdown of Smad2 enhances neurogenesis and the transcription of Smad3-specific targets. A mathematical model of the TGF-b pathway fits the experimental results and predicts that the proportions of the three different trimeric complexes formed dictates the transcriptional responses of the R-Smad proteins. As such, Smad2 targets are activated solely by the Smad2-Smad2-Smad4 complex, whereas Smad3 targets are activated both by Smad2-Smad3-Smad4 and Smad3-Smad3-Smad4 trimers. We have modeled the Smad responses onto arbitrary genes and propose that this mechanism might be extended to additional activities of TGF-b in development and disease.

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smad2 and smad3 Are Required for Mesendoderm Induction by Transforming Growth Factor-β/Nodal Signals in Zebrafish

Cited by 55 publications

References 49 publications

Smad2 mediates Activin/Nodal signaling in mesendoderm differentiation of mouse embryonic stem cells

Smad2 mediates Activin/Nodal signaling in mesendoderm differentiation of mouse embryonic stem cells

Ror2 Receptor Mediates Wnt11 Ligand Signaling and Affects Convergence and Extension Movements in Zebrafish

Smad2 and Smad3 cooperate and antagonize simultaneously in vertebrate neurogenesis

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