Liu G, Kuwayama H, Ishida S, Newell P C
Department of Biochemistry, University of Oxford, UK.
J Cell Sci. 1993 Oct;106 ( Pt 2):591-5. doi: 10.1242/jcs.106.2.591.
Evidence has previously been reported that, during chemotaxis of the cellular slime mould Dictyostelium discoideum, cyclic GMP regulates the association of myosin II with the cytoskeleton and that this regulation is effected by inhibiting myosin II heavy chain phosphorylation (Liu and Newell, J. Cell Sci., 90, 123-129, 1988; 98, 483-490, 1991). Here we provide further evidence in support of this hypothesis using a mutant (KI-10) that is defective in chemotaxis and lacks the normal cyclic AMP-induced cyclic GMP response. We found that the cyclic AMP-induced cytoskeletal actin response was similar to that of the parental strain in this mutant (although showing a slight displacement in the dose-response curve) but the cytoskeletal myosin II heavy chain response was abolished. Moreover, the mutant showed no phosphorylation of myosin II heavy chain in response to cyclic AMP. Compared to the parental strain XP55, the mutant cells contained approximately 40% more protein and their doubling time was 30% longer. These differences could be due to differences in the efficiency of cell division, a process in which the proper regulation of myosin function is essential and in which cyclic GMP may therefore play a role.
先前已有证据报道，在细胞黏菌盘基网柄菌的趋化作用过程中，环鸟苷酸（cGMP）调节肌球蛋白II与细胞骨架的结合，并且这种调节是通过抑制肌球蛋白II重链磷酸化来实现的（Liu和Newell，《细胞科学杂志》，90卷，123 - 129页，1988年；98卷，483 - 490页，1991年）。在此，我们使用一种在趋化作用方面存在缺陷且缺乏正常环磷酸腺苷（cAMP）诱导的环鸟苷酸反应的突变体（KI - 10），提供了进一步支持该假设的证据。我们发现，在该突变体中，环磷酸腺苷诱导的细胞骨架肌动蛋白反应与亲本菌株相似（尽管在剂量反应曲线中显示出轻微偏移），但细胞骨架肌球蛋白II重链反应被消除。此外，该突变体对环磷酸腺苷无肌球蛋白II重链磷酸化反应。与亲本菌株XP55相比，突变体细胞的蛋白质含量大约多40%，其倍增时间长30%。这些差异可能归因于细胞分裂效率的差异，在这个过程中肌球蛋白功能的正确调节至关重要，因此环鸟苷酸可能在其中发挥作用。
