The myosin I SH3 domain and TEDS rule phosphorylation site are required for in vivo function.
The myosin I SH3 domain and TEDS rule phosphorylation site are required for in vivo function.
复制标题
肌球蛋白 I SH3 结构域和 TEDS 规则磷酸化位点是体内功能所必需的。
DOI：
10.1091/mbc.9.1.75
复制
发表时间：
1998
影响因子：
3.3
通讯作者：
M. Titus
中科院分区：
文献类型：
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作者：
K. D. Novak;M. Titus
I 类肌球蛋白在控制许多不同类型的基于肌动蛋白的细胞运动中发挥着重要作用。缺乏或过度表达变形虫肌球蛋白的盘基网柄菌细胞在皮质活动中具有显着缺陷，例如伪足延伸、细胞迁移和巨胞饮作用。具有强烈表型缺陷的盘基网柄菌无效突变体的存在使得互补分析成为探索肌球蛋白 I 重链重要功能特征的一种手段。缺乏两种肌球蛋白的突变盘基网柄菌细胞在生长、内吞作用和 F-肌动蛋白重排方面表现出严重缺陷。全长 myoB 重链在这些细胞中的表达完全挽救了双突变缺陷。然而，myoB 重链的突变形式（其中共有磷酸化位点处的丝氨酸已被改变为丙氨酸或其中 C 端 SH3 结构域已被去除）无法补充无效表型。当 myoB 重链的野生型和突变型在肌球蛋白 I 无效突变体中表达时，它们似乎被正确定位。这些结果表明，阿米巴肌球蛋白 I 共有磷酸化位点和 SH3 结构域在肌球蛋白 I 的定位中不起作用，但对于体内功能绝对是必需的。
The class I myosins play important roles in controlling many different types of actin-based cell movements. Dictyostelium cells either lacking or overexpressing amoeboid myosin Is have significant defects in cortical activities such as pseudopod extension, cell migration, and macropinocytosis. The existence of Dictyostelium null mutants with strong phenotypic defects permits complementation analysis as a means of exploring important functional features of the myosin I heavy chain. Mutant Dictyostelium cells lacking two myosin Is exhibit profound defects in growth, endocytosis, and rearrangement of F-actin. Expression of the full-length myoB heavy chain in these cells fully rescues the double mutant defects. However, mutant forms of the myoB heavy chain in which a serine at the consensus phosphorylation site has been altered to an alanine or in which the C-terminal SH3 domain has been removed fail to complement the null phenotype. The wild-type and mutant forms of the myoB heavy chain appeared to be properly localized when they were expressed in the myosin I null mutants. These results suggest that the amoeboid myosin I consensus phosphorylation site and SH3 domains do not play a role in the localization of myosin I, but are absolutely required for in vivo function.
Yamagata, H.：“利用短芽孢杆菌有效合成和分泌人表皮生长因子。”
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