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Fig. 5. Even in the absence of dominant inhibitory signals from ExE, induction
of DVE depends on Nodal and proprotein convertase activities. As expected
(Rodriguez et al., 2005),
embryo explants stripped of ExE at the DVE stage (E5.5) induce Lim1
and HexP-GFP throughout the EmVE endoderm (top row). Purified recombinant
Nodal (50 µg/ml) does not prevent ectopic induction of DVE markers (second
row). By contrast, blocking endogenous Nodal activity through inhibition of
its signaling receptors (+SB) or proprotein convertases (+CMK) prevents
ectopic induction of both HexP-GFP and Lim1. Processed Nodal (50
µg/ml) administred to the outer (apical) membrane of the visceral endoderm
is not sufficient to ectopically induce HexP-GFP and Lim1, whereas
processed Activin (50 µg/ml) is (bottom rows). Note that the thickness of
the VE is significantly increased upon inhibition of Nodal signaling compared
with untreated controls or explants treated with Activin. SB, SB-431542 (10
µmol/l); CMK, dec-RVKR-CMK (25 µmol/l).
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