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Fig. 6. Mammary outgrowth is defective in E2F mutant mice. (A)
Wholemounts from wild-type, E2f1-knockout, E2f3 heterozygous
and E2f4-knockout mice are shown at 4 and 8 weeks of age. (B)
The extent of mammary epithelial outgrowth was quantitated at 4 weeks of
development. Relative to the control, there was a significant difference in
E2f1-knockout (P=0.0017), E2f3 heterozygous
(P<0.0001) and E2f4-knockout (P<0.0001) mice.
This outgrowth analysis was repeated at 8 weeks of age, when the
E2f3-knockout and E2f4-knockout exhibit a growth delay
(P=0.059 and P=0.02, respectively) relative to the control.
In addition, ductal branching was quantitated at 8 weeks and was significant
for each of the E2F mutant strains, except the E2f2-knockout mice
[P=0.05 (E2f1), 0.00008 (E2f3 heterozygous), 0.0003
(E2f3 knockout) and 0.001 (E2f4 knockout)]. (C)
Transplants of control and E2F mutant mammary epithelium in nu/nu recipients
as shown in a wholemount analysis. (D) Quantitation of transplant
outgrowth in E2F mutants relative to wild-type control. E2f1-knockout
ductal extension was reduced (to 74% of control, P=0.046), whereas no
defects were observed for E2f2 knockouts. E2f3-knockout and
E2f3 heterozygous mice had 36% (P=0.014) and 78% growth
(P=0.043), respectively, of wild-type growth. E2f4 knockouts
were most severely affected with only 23% of control growth
(P=0.010). Asterisk denotes statistical significance.
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