IONIC MECHANISMS IN THE REGULATION OF MITOSIS

我们将记录和调查变化的作用， 细胞内游离钙在有丝分裂中的作用 它们在控制细胞结构中发挥作用。 我们发现 核膜内游离钙增加 在有丝分裂过程中， 海胆胚胎的快速卵裂期和细胞分裂期 组织培养中动物细胞的分裂。 为了扩展这项工作，我们 将对细胞进行视觉观察， 钙的测量是为了精确地指出 与结构事件的关系，无论是在时间上还是在两个- 细胞中游离钙分布的三维图像。 我们 将试图阻止细胞周期的进展， 包膜破裂和在中/后期的过渡 通过控制钙从外部进入动物细胞或通过 微量注射钙降低细胞内游离钙 缓冲器。 我们对抗体的初步研究结果表明 正常进展中的Ca 2 +/钙调素依赖性蛋白激酶 通过核爆 我们会把这些 研究包括中期后期过渡，并试图 在两个点重新启动有丝分裂，形成非钙依赖型 当有丝分裂被低钙抑制时， 缓冲器。

We will document and investigate the role of changes in intracellular free calcium during mitosis to determine what role they play in controlling cell structure. We have found that intracellular free calcium increases at nuclear envelope breakdown and at the onset of anaphase during mitosis both during the rapid cleavage stage of the sea urchin embryo and during cell division in animal cells in tissues culture. To extend this work we will make visual observations of the cell at the same time the calcium measurements are taken to pin-point the exact relationship to the structural events, both in time and in two- dimensional images of free calcium distribution in the cell. We will attempt to block progression of the cell cycle at nuclear envelope breakdown and at the metaphaseanaphase transition in animal cells by controlling calcium entry from outside or by lowering intracellular free calcium with microinjected calcium buffers. Our preliminary results with anti-bodies have implicated Ca2+/calmodulin-dependent protein kinase in normal progression through nuclear envelop breakdown. We will extend these these studies to include the meta-anaphase transition and try to reinitiate mitosis at both points with calcium-independent forms of this enzyme when mitoses has been arrested by low calcium buffers.