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. 2009 Feb 3;7(2):e1000029. doi: 10.1371/journal.pbio.1000029

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This is an open-access article distributed under the terms of the Creative Commons Public Domain declaration which stipulates that, once placed in the public domain, this work may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose.

This is an open-access article distributed under the terms of the Creative Commons Public Domain declaration, which stipulates that, once placed in the public domain, this work may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose.

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Individual blastomeres of embryos were injected as diagrammed to the left and analyzed by two-color FISH for gfp (red) and endo16 (green) transcripts. The concentrations of gfp mRNA, pmar1 mRNA, and ActivinB-MO1 used were 0.5 μg/μl, 0.2 μg/μl, and 1.4 mM, respectively. The presence of ActivinB MO1 in Pmar1-expressing cells (f–j) strongly inhibits ectopic and not endogenous (arrowheads in i and j) endo16 mRNA expression in the uninjected half of the embryo. When ActivinB MO1 is injected exclusively into blastomeres that respond to Pmar1-dependent induction (k–o), both ectopic and endogenous endo16 mRNA expression are strongly reduced. At the mesenchyme blastula stage shown, Pmar1 (gfp)-expressing cells in c, h, m and b, g, l acquire mesenchymal character and ingress into the blastocoel. Images represent the phenotypes observed in 16/19 (a–e), 43/47 (f–j), and 6/6 (k–o) injected embryos.