Click here to close Hello! We notice that you are using Internet Explorer, which is not supported by Xenbase and may cause the site to display incorrectly. We suggest using a current version of Chrome, FireFox, or Safari.
XB-IMG-47180

Xenbase Image ID: 47180


Figure 1. Xenopus E-Syt2 Is Required for Induction of the Early Mesoderm Gene Xbra and for FGF Signaling(A) Predicted structural domains of E-Syt2 orthologs, “x” Xenopus, “h” human, “Dm” Drosophila melanogaster, “Ce” Caenorhabditis elegans.(B) Zygotic E-Syt2 expression depends on FGF signaling. FGF signaling was inhibited by the expression of the dominant-negative FGF receptor “XFD” (100, 200, and 400 pg) in ventral marginal zone (VMZ) explants.(C) In vivo Xbra expression is suppressed by E-Syt2 depletion. Dorsal blastomeres of four cell embryos were each injected equatorially with 0.75 pmol of Mo-C and increasing amounts of HA-E-Syt2 mRNA and Xbra expression at stage 10.5 revealed by whole-mount in situ hybridization.(D) E-Syt2 depletion suppresses ectopic induction of Xbra by activated FGFR1. Embryos were injected with 0.9 or 1.8 pmol Mo-B or Ctrl Mo and with 2.5 pg constitutively active FGFR1 (CA-FGFR1) or 5 pg VRas.(E) Activated FGFR1 (1.5 pg/cell, four cell embryos) induction of ectopic ERK activation in ACs was also suppressed by depletion of E-Syt2 (3 pmol MoC/cell).(F) Depletion of E-Syt2 also suppresses FGF8-dependent differentiation. Embryos were unilaterally coinjected with FGF8 (2.5 pg), β-galactosidase (325 pg) mRNAs, and E-Syt2 Mo-B or Ctrl Mo (2 pmol) and subjected to whole-mount in situ to reveal N-tubulin expression (blue). Purple staining (β-galactosidase activity assay) indicates injected side of embryo.See also Figure S1.

Image published in: Jean S et al. (2010)

Copyright © 2010. Image reproduced with permission of the Publisher, Elsevier B. V.

GeneSynonymsSpeciesStage(s)Tissue
tbxt.Lbra, brachyury, ntl, t, t-a, t-b, X-bra, Xbra, XbrachyuryX. laevisThroughout NF stage 10.5mesoderm
marginal zone

Image source: Published

Larger Image
Printer Friendly View

Return to previous page