E2F1 and p53 are dispensable, whereas p21(Waf1/Cip1) cooperates with Rb to restrict endoreduplication and apoptosis during skeletal myogenesis.
摘要:
We describe temporal and genetic analyses of partially rescued Rb mutant fetuses, mgRb:Rb-/-, that survive to birth and reveal specific defects in skeletal muscle differentiation. We show that in the absence of Rb, these fetuses exhibit increased apoptosis, bona fide endoreduplication, and incomplete differentiation throughout terminal myogenesis. These defects were further augmented in composite mutant fetuses, mgRb:Rb-/-:p21-/-, lacking both Rb and the cyclin-dependent kinase inhibitor p21(Waf1/Cip1). Although E2F1 and p53 mediate ectopic DNA synthesis and cell death in several tissues in Rb mutant embryos, both endoreduplication and apoptosis persisted in mgRb:Rb-/-:E2F1-/- and mgRb:Rb-/-:p53-/- compound mutant muscles. Thus, combined inactivation of Rb and p21(Waf1/Cip1) augments endoreduplication and apoptosis, whereas E2F1 and p53 are dispensable during aberrant myogenesis in Rb-deficient fetuses.
收起
展开
DOI:
10.1006/dbio.2000.9892
被引量:
年份:
2000


通过 文献互助 平台发起求助,成功后即可免费获取论文全文。
求助方法1:
知识发现用户
每天可免费求助50篇
求助方法1:
关注微信公众号
每天可免费求助2篇
求助方法2:
完成求助需要支付5财富值
您目前有 1000 财富值
相似文献(205)
参考文献(0)
引证文献(15)
来源期刊
影响因子:3.145
JCR分区: 暂无
中科院分区:暂无