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. Author manuscript; available in PMC: 2013 Apr 3.
Published in final edited form as: Development. 2008 Jun 11;135(14):2403–2413. doi: 10.1242/dev.019018

Fig. 6. Mammary outgrowth is defective in E2F mutant mice.

Fig. 6

(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.