Wang Y, Liu J, Segall J E
Department of Anatomy, Albert Einstein College of Medicine, Bronx, NY 10461, USA.
J Cell Sci. 1998 Feb;111 ( Pt 3):373-83. doi: 10.1242/jcs.111.3.373.
Mutants lacking the MAP kinase DdERK2 show reduced chemotactic responses to folate and cAMP. Analysis of cAMP chemotaxis shows that Dderk2- cells are defective in chemotaxis to high concentrations of cAMP. This defect is due to an inability to repolarize in the continued presence of high concentrations of cAMP. Under these conditions, the speed of movement of mutant cells remains low. Instead of generating a leading pseudopod, mutant cells generate transient crown-like structures over multiple regions of the cell surface. These structures differ from pseudopods in that they contain myosin II as well as F actin and coronin. These studies identify a role for MAP kinases in coordinating the formation of cell projections generated in response to chemoattractants.
缺乏丝裂原活化蛋白激酶DdERK2的突变体对叶酸和环磷酸腺苷（cAMP）的趋化反应降低。对cAMP趋化性的分析表明，Dderk2-细胞在对高浓度cAMP的趋化作用中存在缺陷。这种缺陷是由于在高浓度cAMP持续存在的情况下无法重新极化。在这些条件下，突变细胞的移动速度仍然很低。突变细胞不是产生一个领先的伪足，而是在细胞表面的多个区域产生短暂的冠状结构。这些结构与伪足的不同之处在于它们含有肌球蛋白II以及F肌动蛋白和冠蛋白。这些研究确定了丝裂原活化蛋白激酶在协调响应化学引诱剂而产生的细胞突起形成中的作用。
