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Fig. 3. Vascular defects in Mib1–/– embryos. (A-D)
Whole-mount Flk1 antibody staining of E9.0 wild-type (A,C) and
Mib1–/– (B,D) embryos.
Mib1–/– embryos have relatively thin and
disorganized blood vessels. (A,B) Lateral view of the head; (C,D) Dorsal view
of the trunk. (E-N) Transverse sections of E9.0 wild-type (E,G,I,K,M) and
Mib1–/– (F,H,J,L,N) embryos, stained with an
anti-PECAM antibody (E,F) or labeled by in situ hybridization with specific
probes for ephrin B2 (G,H), Sm22 (I,J), Dll4 (K,L) and
Hey1 (M,N). The PECAM-stained sections revealed the marked reduction
or loss of the dorsal aorta (da) in the
Mib1–/– embryos. The lack of vascular ephrin
B2 expression (H; inset), smooth muscle cell recruitment (J; inset), and
Hey1 expression (N; inset) in the
Mib1–/– embryos is evident, whereas the
Dll4 expression is normal (L; inset). (O,P) Expression of vascular
Notch target genes (Hey1 and Hey2) and genes for
vasculogenesis (ephrin B2, EphB4, Vegf and Shh). Total RNA
from E9.0 wild-type and Mib1–/–yolk sacs was
analyzed by semi-quantitative RT-PCR (O). The expression of Hey1 and
Hey2 was analyzed by real-time quantitative RT-PCR (P). The numbers
on each bar indicate the mean fold of induction, and the error bars indicate
the standard deviation. ß-actin was used for normalization. The results
are representative of three independent experiments. ***P<0.0001,
*P<0.01.
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