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Disruption of calvarial ossification in E2f4 mutant embryos correlates with increased proliferation and progenitor cell populations

机译：E2f4突变胚胎中颅骨骨化的破坏与增殖和祖细胞群增加有关

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摘要

The E2F family of transcription factors, in association with pocket protein family members, are important for regulating genes required for cellular proliferation. The most abundant E2F, E2F4, is implicated in maintaining the G0/G1 cell cycle state via transcriptional repression of genes that encode proteins required for S-phase progression. Here, we investigate E2F4's role in bone development using E2f4 germline mutant mice. We find that mutation of E2f4 impairs the formation of several bones that arise through intramembranous or endochondral ossification. The most severe defect occurred in the calvarial bones of the skull where we observed a striking delay in their ossification. In vivo and in vitro analyses established that E2F4 loss did not block the intrinsic differentiation potential of calvarial osteoblast progenitors. However, our data showed that E2f4 mutation elevated proliferation in the developing calvaria in vivo and it increased the endogenous pool of undifferentiated progenitor cells. These data suggest that E2F4 plays an important role in enabling osteoblast progenitors to exit the cell cycle and subsequently differentiate thereby contributing to the commitment of these cells to the bone lineage.
机译：E2F转录因子家族与口袋蛋白家族成员相关，对于调节细胞增殖所需的基因很重要。最丰富的E2F，E2F4通过编码S期进程所需蛋白的基因的转录抑制来维持G0 / G1细胞周期状态。在这里，我们调查了E2F4在使用E2f4种系突变小鼠的骨骼发育中的作用。我们发现，E2f4的突变会损害通过膜内或软骨内骨化引起的几个骨骼的形成。最严重的缺陷发生在颅骨的颅骨，我们观察到它们的骨化明显延迟。体内和体外分析表明，E2F4的丧失并没有阻止颅骨成骨祖细胞的内在分化潜能。但是，我们的数据显示E2f4突变可提高体内发育中的颅骨的增殖，并增加未分化祖细胞的内源库。这些数据表明，E2F4在使成骨细胞祖细胞退出细胞周期并随后分化中起着重要作用，从而有助于这些细胞向骨谱系的定向。

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