Pons S, Trejo J L, Martínez-Morales J R, Martí E
Instituto Cajal de Neurobiología, CSIC, Av. Doctor Arce 37, Madrid E28002, Spain.
Development. 2001 May;128(9):1481-92. doi: 10.1242/dev.128.9.1481.
During development of the cerebellum, Sonic hedgehog (SHH) is expressed in migrating and settled Purkinje neurons and is directly responsible for proliferation of granule cell precursors in the external germinal layer. We have previously demonstrated that SHH interacts with vitronectin in the differentiation of spinal motor neurons. Here, we analysed whether similar interactions between SHH and extracellular matrix glycoproteins regulate subsequent steps of granule cell development. Laminins and their integrin receptor subunit alpha6 accumulate in the outer most external germinal layer where proliferation of granule cell precursors is maximal. Consistent with this expression pattern, laminin significantly increases SHH-induced proliferation in primary cultures of cerebellar granule cells. Vitronectin and its integrin receptor subunits alpha(v) are expressed in the inner part of the external germinal layer where granule cell precursors exit the cell cycle and commence differentiation. In cultures, vitronectin is able to overcome SHH-induced proliferation, thus allowing granule cell differentiation. Our studies indicate that the pathway in granule cell precursors responsible for the conversion of a proliferative SHH-mediated response to a differentiation signal depends on CREB. Vitronectin stimulates phosphorylation of cyclic-AMP responsive element-binding protein (CREB), and over-expression of CREB is sufficient to induce granule cell differentiation in the presence of SHH. Taken together, these data suggest that granule neuron differentiation is regulated by the vitronectin-induced phosphorylation of CREB, a critical event that terminates SHH-mediated proliferation and permits the differentiation program to proceed in these cells.
在小脑发育过程中,音猬因子(SHH)在迁移和定居的浦肯野神经元中表达,并且直接负责外颗粒层中颗粒细胞前体的增殖。我们之前已经证明,SHH在脊髓运动神经元的分化过程中与玻连蛋白相互作用。在此,我们分析了SHH与细胞外基质糖蛋白之间的类似相互作用是否调节颗粒细胞发育的后续步骤。层粘连蛋白及其整合素受体亚基α6在颗粒细胞前体增殖最为旺盛的最外层外颗粒层中积累。与这种表达模式一致,层粘连蛋白在小脑颗粒细胞原代培养物中显著增加SHH诱导的增殖。玻连蛋白及其整合素受体亚基α(v)在外颗粒层内部表达,颗粒细胞前体在此处退出细胞周期并开始分化。在培养物中,玻连蛋白能够克服SHH诱导的增殖,从而使颗粒细胞分化。我们的研究表明,颗粒细胞前体中负责将增殖性SHH介导的反应转化为分化信号的途径依赖于CREB。玻连蛋白刺激环磷酸腺苷反应元件结合蛋白(CREB)的磷酸化,并且在存在SHH的情况下,CREB的过表达足以诱导颗粒细胞分化。综上所述,这些数据表明颗粒神经元的分化受玻连蛋白诱导的CREB磷酸化调节,这是一个关键事件,它终止了SHH介导的增殖并允许这些细胞中的分化程序继续进行。