Dynacortin, a genetic link between equatorial contractility and global shape control discovered by library complementation of a Dictyostelium discoideum cytokinesis mutant.
Dynacortin, a genetic link between equatorial contractility and global shape control discovered by library complementation of a Dictyostelium discoideum cytokinesis mutant.
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DynAcortin是赤道收缩力与图书馆distecoideum cytokinesis突变体发现的赤道收缩力与全球形状控制之间的遗传联系。
DOI：
10.1083/jcb.150.4.823
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发表时间：
2000-08-21
影响因子：
7.8
通讯作者：
Spudich, J A
中科院分区：
文献类型：
--
作者：
Robinson, D N;Spudich, J A
我们已经开发了一个系统进行交互遗传学的Dictyosteelium discoideum，使用cDNA文库互补/多拷贝抑制策略。筛选化学诱变的细胞中的胞内分裂缺陷突变体，并对一种突变体进行文库互补。四种不同基因的分离物被回收作为该菌株胞质分裂缺陷的修饰物。这些包括切割沟蛋白皮质素I，一种我们命名为dynacortin的新蛋白质，一种ezrin-radixin-moesin家族蛋白质，以及冠蛋白。发现在菌株中皮质素I基因座和转录物被破坏，将其鉴定为受影响的基因。Dynacortin部分定位于细胞皮质，并在肿胀区域富集，这是一种类似于冠状蛋白的定位模式，部分依赖于RacE。在胞质分裂期间，在皮质中发现了动力皮质素，并且在两极有所富集。此外，它似乎在卵裂沟中减少。的遗传相互作用和细胞分布的蛋白质提出了一个假说，胞质分裂中的内侧环的收缩是一个功能的空间限制皮质素I和肌球蛋白II和全球分布的dynacortin，冠状蛋白，和种族。
We have developed a system for performing interaction genetics in Dictyostelium discoideum that uses a cDNA library complementation/multicopy suppression strategy. Chemically mutagenized cells were screened for cytokinesis-deficient mutants and one mutant was subjected to library complementation. Isolates of four different genes were recovered as modifiers of this strain's cytokinesis defect. These include the cleavage furrow protein cortexillin I, a novel protein we named dynacortin, an ezrin-radixin-moesin-family protein, and coronin. The cortexillin I locus and transcript were found to be disrupted in the strain, identifying it as the affected gene. Dynacortin is localized partly to the cell cortex and becomes enriched in protrusive regions, a localization pattern that is similar to coronin and partly dependent on RacE. During cytokinesis, dynacortin is found in the cortex and is somewhat enriched at the poles. Furthermore, it appears to be reduced in the cleavage furrow. The genetic interactions and the cellular distributions of the proteins suggest a hypothesis for cytokinesis in which the contraction of the medial ring is a function of spatially restricted cortexillin I and myosin II and globally distributed dynacortin, coronin, and RacE.