Fig. 3. Wild-type xTsg and the hyperventralizing mutant xTsgW67G antagonize the dorsalization of mesoderm by Activin. (A-D) Animal cap explants were isolated at stage 8 and treated with 2 ng/ml Activin protein. Activin induces elongation (B). Microinjection of a total of 2 ng xTsg (C) or xTsgW67G (D) mRNA at the eight-cell stage into the animal blastomeres prevented elongation. (E) The accumulation of Activin-induced endogenous Chordin protein (lane 2) was reduced by wild-type xTsg mRNA injection (lane 3) and increased by xTsgW67G (lane 4). (F) RT-PCR analysis of animal cap explants treated with Activin after microinjection of 2 ng xTsg or xTsgW67G mRNA; both mRNAs inhibited the induction of dorsal mesodermal (MyoD, alpha-Actin) or neural (NCAM) marker genes by Activin. EF1α served as a loading control.
Image published in: Oelgeschläger M et al. (2003)
Copyright © 2003. Image reproduced with permission of the publisher and the copyright holder. This is an Open Access article distributed under the terms of the Creative Commons Attribution License.
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