Identification of a novel tubulin-destabilizing protein related to the chaperone cofactor E
Identification of a novel tubulin-destabilizing protein related to the chaperone cofactor E
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DOI：
10.1242/jcs.01719
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发表时间：
2005-03-15
影响因子：
4
通讯作者：
Cowan, NJ
中科院分区：
文献类型：
--
作者：
Bartolini, F;Tian, GL;Cowan, NJ
调节微管细胞骨架的因素是决定细胞行为的关键。在这里，我们描述了一种新的蛋白质的功能，我们称之为E-like，因为它与微管蛋白特异的伴侣辅助因子E的序列相似。我们发现，在过度表达时，E-like通过将微管蛋白转化为蛋白酶体降解来解聚微管。我们的数据表明，这一功能是直接的，并基于E-like在体外破坏微管蛋白异源二聚体的能力。抑制E-like的表达导致稳定的微管数量增加，细胞内膜紧密聚集在微管组织中心周围，而动态微管的性质不受影响。这些观察将E-like定义为微管蛋白稳定性的一种新的调节因子，并在微管蛋白周转和囊泡运输之间提供了联系。
Factors that regulate the microtubule cytoskeleton are critical in determining cell behavior. Here we describe the function of a novel protein that we term E-like based on its sequence similarity to the tubulin-specific chaperone cofactor E. We find that upon overexpression, E-like depolymerizes microtubules by committing tubulin to proteosomal degradation. Our data suggest that this function is direct and is based on the ability of E-like to disrupt the tubulin heterodimer in vitro. Suppression of E-like expression results in an increase in the number of stable microtubules and a tight clustering of endocellular membranes around the microtubule-organizing center, while the properties of dynamic microtubules are unaffected. These observations define E-like as a novel regulator of tubulin stability, and provide a link between tubulin turnover and vesicle transport.