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Fig. 5. Endocardial inactivation of Tgfß signaling causes DILV.
(A,B) Whole-mount examination of E12.5 embryonic hearts from a
control (A) and a mutant (B) embryo stained with X-gal. Red arrows show the
interventricular sulcus at the apex of the heart. (C-H) Frontal
sections of E12.5 hearts from control (C,F) or mutant (D,E,G,H) embryos
stained with X-gal. Asterisks in C and D indicate the mesenchymal cap of the
ASP. E represents the dark field view of D. Owing to penetration problems,
which are common in X-gal staining studies, results of X-gal staining of E12.5
embryonic hearts varied dramatically among samples. X-gal staining products
appear pink in the dark field, and can be detected more easily than in the
bright field. Arrows in G indicate that both the right atrium (RA) and left
atrium (LA) empty through separated `inlets' to the left ventricle, resulting
in a DILV defect. (I) The relative cushion sizes of mutant embryonic
hearts versus control hearts were measured as described in the Materials and
methods. #P<0.05. (J-L) Cross sections of E12.5
hearts from control (J) and mutant (K,L) embryos show normal growth of the
right ventricle. The section in K is close to the apex of the heart, and the
section in L is at the level at which the VSD (black arrow) is obvious.
(M) The size of the right ventricle is approximately the same as the
left ventricle in both control and mutant embryos. (N-Q) Section in
situ hybridization analysis performed on sagittally sectioned embryos
(E9.5-E11.5) with a [35S]-labeled antisense probe (N-P)
corresponding to the first four exons of Tgfbr2, or a sense probe as
a negative control (Q). ASP, atrial septum premium; cko,
Tie2cre;Tgfbr2loxp/loxp;R26R; ctrl,
Tie2cre;Tgfbr2loxp/+;R26R; IC, inferior endocardial
cushion; LA, left atrium; LV, left ventricle; RA, right atrium; RV, right
ventricle; SC, superior endocardial cushion.
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