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Fig. 2. Nkx2.5Cre activity and tissue-specific inactivation of
Bmp2 in mouse embryos. (A) At 8.5 dpc, Nkx2.5Cre activity is
visualized throughout the heart (ventral view in A). (B) At 9.5 dpc,
parasagittal sections indicated there is intense ß-gal activity in both
myocardium (arrow) and endocardium (arrowhead). (C-J). In-situ analysis using
Bmp2 exon 3 as a probe, showing that at 8.5 dpc Bmp2 is
expressed in the sinus venosus in the wild-type embryo (arrow, C) and is still
expressed in the mutant (arrow, D). At 9.0 dpc (E,F) and 9.5 dpc (G,H,I,J),
Bmp2 is highly expressed in the myocardium of the control AV canal
(arrow, E,G,I) but is absent in the Bmp2 CKO mutant (arrow, F,H,J). I
and J are parasagittal sections of embryos in G and H. (K,L)
Immunohistochemistry of phospho-Smad1/5/8, effectors of Bmp signaling,
indicating Bmp-responding cells in the endocardium (denoted by arrow) and
myocardial cells (arrowhead) of the AV canal at 9.5 dpc (K). In the
Bmp2 CKO mutant, the phospho-Smad 1/5/8 signal is reduced in both
cell populations (L). a, atrium; ba, branchial arch; fn, fronto-nasal process;
hf, head fold; sv, sinus venosus; v, ventricle.
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