Humbert P O, Rogers C, Ganiatsas S, Landsberg R L, Trimarchi J M, Dandapani S, Brugnara C, Erdman S, Schrenzel M, Bronson R T, Lees J A
Department of Biology, Massachusetts Institute of Technology, Cambridge 02139, USA.
Mol Cell. 2000 Aug;6(2):281-91. doi: 10.1016/s1097-2765(00)00029-0.
The retinoblastoma protein (pRB) plays a key role in the control of normal development and proliferation through the regulation of the E2F transcription factors. We generated a mutant mouse model to assess the in vivo role of the predominant E2F family member, E2F4. Remarkably, loss of E2F4 had no detectable effect on either cell cycle arrest or proliferation. However, E2F4 was essential for normal development. E2f4-/- mice died of an increased susceptibility to opportunistic infections that appeared to result from craniofacial defects. They also displayed a variety of erythroid abnormalities that arose from a cell autonomous defect in late stage maturation. This suggests that E2F4 makes a major contribution to the control of erythrocyte development by the pRB tumor suppressor.
视网膜母细胞瘤蛋白（pRB）通过调控E2F转录因子，在正常发育和增殖的控制中发挥关键作用。我们构建了一个突变小鼠模型，以评估主要的E2F家族成员E2F4在体内的作用。值得注意的是，E2F4的缺失对细胞周期停滞或增殖均未产生可检测到的影响。然而，E2F4对正常发育至关重要。E2f4-/-小鼠死于对机会性感染易感性增加，这似乎是由颅面缺陷导致的。它们还表现出多种红细胞异常，这些异常源于晚期成熟过程中的细胞自主性缺陷。这表明E2F4对pRB肿瘤抑制因子控制红细胞发育起主要作用。
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