Differentiation of cultured skeletal myoblasts is induced by extrinsic signals that include reduction in ambient mitogen concentration and increased cell density. Using an established murine myoblast cell line (C2C12), we have found that experimental reduction of the nucleoporin p62 (Nup62) content of myoblasts enhances differentiation in high-mitogen medium, while forced expression of Nup62 inhibits density-induced differentiation. In contrast, differentiation of myoblasts induced by low-mitogen medium was unaffected by ectopic Nup62 expression. Further analyses suggested that Nup62 content affects density-induced myoblast differentiation through a mechanism involving activation of p38 MAP kinase. Nuclear pore complex (NPC) composition, in particular changes in NUP62 content, may be altered during viral infection, differentiation, and in neoplastic growth. The results support a functional role for changes in Nup62 composition in NPCs and density-induced myogenic differentiation, and suggest a link between loss of Nup62 content and induction of an intracellular stress signaling pathways.

培养的骨骼肌成肌细胞的分化是由外在信号引起的，外在信号包括环境有丝分裂原浓度的降低和细胞密度的增加。使用已建立的鼠成肌细胞系（C2C12），我们发现实验性降低成肌细胞核仁素p62（Nup62）含量可增强高促分裂原培养基中的分化，而Nup62的强制表达则可抑制密度诱导的分化。相比之下，异位Nup62表达不影响低促分裂原培养基诱导的成肌细胞分化。进一步的分析表明，Nup62含量通过涉及p38 MAP激酶激活的机制影响密度诱导的成肌细胞分化。核孔复合物（NPC）的组成，尤其是NUP62含量的变化，可能在病毒感染，分化，和肿瘤生长。该结果支持NPC中Nup62组成的变化和密度诱导的肌原性分化的功能性作用，并暗示了Nup62含量的减少与细胞内应激信号通路的诱导之间的联系。