Zhang J M, Wei Q, Zhao X, Paterson B M
Laboratory of Biochemistry, NCI, National Institutes of Health, Building 37 Room 4A21, 9000 Rockville Pike, Bethesda, MD 20892, USA.
EMBO J. 1999 Feb 15;18(4):926-33. doi: 10.1093/emboj/18.4.926.
Proliferating myoblasts express the muscle determination factor, MyoD, throughout the cell cycle in the absence of differentiation. Here we show that a mitogen-sensitive mechanism, involving the direct interaction between MyoD and cdk4, restricts myoblast differentiation to cells that have entered into the G0 phase of the cell cycle under mitogen withdrawal. Interaction between MyoD and cdk4 disrupts MyoD DNA-binding, muscle-specific gene activation and myogenic conversion of 10T1/2 cells independently of cyclin D1 and the CAK activation of cdk4. Forced induction of cyclin D1 in myotubes results in the cytoplasmic to nuclear translocation of cdk4. The specific MyoD-cdk4 interaction in dividing myoblasts, coupled with the cyclin D1-dependent nuclear targeting of cdk4, suggests a mitogen-sensitive mechanism whereby cyclin D1 can regulate MyoD function and the onset of myogenesis by controlling the cellular location of cdk4 rather than the phosphorylation status of MyoD.
增殖的成肌细胞在未分化的整个细胞周期中都表达肌肉决定因子MyoD。在此我们表明,一种有丝分裂原敏感机制,涉及MyoD与cdk4之间的直接相互作用,将成肌细胞分化限制在有丝分裂原撤除后进入细胞周期G0期的细胞中。MyoD与cdk4之间的相互作用破坏了MyoD的DNA结合、肌肉特异性基因激活以及10T1/2细胞的成肌转化,这与细胞周期蛋白D1和cdk4的CAK激活无关。在肌管中强制诱导细胞周期蛋白D1会导致cdk4从细胞质向细胞核易位。分裂的成肌细胞中MyoD与cdk4的特异性相互作用,以及细胞周期蛋白D1依赖的cdk4核靶向,提示了一种有丝分裂原敏感机制,即细胞周期蛋白D1可通过控制cdk4的细胞定位而非MyoD的磷酸化状态来调节MyoD功能和成肌作用的起始。