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Fig. 8. Ccm1 lies genetically upstream of Notch signaling and
downstream of Vegf. (A-F) Whole-mount in situ hybridization of
Ccm1+/+ and Ccm1-/- tissues at E8.5,
before the mutant phenotype can be distinguished grossly. (A-D) Disruption of
arterial Notch gene expression is demonstrated using probes for
Dll4 and Notch4. (A,B) Hybridization with a probe for the
Notch ligand Dll4 shows marked downregulation of
Dll4 transcript throughout the dorsal aorta of
Ccm1-/- embryos, compared with normal controls. (C,D) A
decrease in Notch4 transcript is evident in the branchial arch artery
and proximal aorta of a Ccm1-/- embryo. The
Notch4 signal intensity was similar, although weak, for the caudal
aorta of both the wild type and the mutant. (E,F) In situ hybridization with a
probe for Vegfa shows a similar intensity of ubiquitous signal from
both Ccm1+/+ and Ccm1-/- embryos. (G)
Quantification of transcript levels by real-time quantitative PCR at E8.8.
Comparison of three pairs of Ccm1+/+ and
Ccm1-/- embryo cDNA samples confirmed downregulation of
Efnb2 expression (despite intact extravascular domains of expression
shown in Fig. 7A-D). Marked
downregulation of Dll4 with modest downregulation of Notch4
was also observed, in agreement with the in situ hybridization data.
Transcript levels for Vegfa were similar between genotypes.
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