The microtubule plus end-tracking proteins mal3p and tip1p cooperate for cell-end targeting of interphase microtubules
The microtubule plus end-tracking proteins mal3p and tip1p cooperate for cell-end targeting of interphase microtubules
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DOI：
10.1016/j.cub.2004.03.029
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发表时间：
2004-04-06
期刊：
影响因子：
9.2
通讯作者：
Brunner, D
中科院分区：
文献类型：
--
作者：
Busch, KE;Brunner, D
背景：CLIP - 170和EB1蛋白家族成员定位于生长中的微管末端，并将空间信息与微管动力学的控制联系起来。目前尚不清楚这些蛋白是独立发挥作用还是其作用是相互协调的。在裂殖酵母中，CLIP - 170的同源物tip1p是微管靶向细胞末端所必需的，而EB1的同源物mal3p在微管组织中的作用尚未被研究。
结果：我们发现mal3p促进微管生长的起始并抑制灾变（微管生长的突然停止和收缩）。在没有mal3p的情况下，过早的灾变在细胞内随机发生。mal3p修饰整个微管晶格，并定位于沿微管及其生长末端的颗粒上。颗粒沿两个方向移动，向细胞末端的外向移动或向细胞中心的内向移动。在细胞末端，与微管末端相关的mal3p颗粒消失，随后发生灾变。mal3p在缺失tip1的细胞中正常定位，并在过早灾变之前从微管末端消失。相反，tip1p需要mal3p才能定位在微管末端。mal3p和tip1p在体外直接相互作用。
结论：mal3p和tip1p形成一个使微管能够靶向细胞末端的系统。我们提出mal3p通过抑制灾变来刺激生长起始并维持生长。在细胞末端，mal3p从微管末端消失，随后发生灾变。mal3p参与将tip1p招募到微管末端。当微管在细胞末端之外接触细胞皮质时，这一点变得很重要，因为没有tip1p时mal3p会过早解离，随后发生过早的灾变。
Background: CLIP-170 and EB1 protein family members localize to growing microtubule tips and link spatial information with the control of microtubule dynamics. It is unknown whether these proteins operate independently or whether their actions are coordinated. In fission yeast the CLIP-170 homolog tip1p is required for targeting of microtubules to cell ends, whereas the role of the EB1 homolog mal3p in microtubule organization has not been investigated.Results: We show that mal3p promotes the initiation of microtubule growth and inhibits catastrophes. Premature catastrophes occur randomly throughout the cell in the absence of mal3p. mal3p decorates the entire microtubule lattice and localizes to particles along the microtubules and at their growing tips. Particles move in two directions, outbound toward the cell ends or inbound toward the cell center. At cell ends, the microtubule tip-associated mal3p particles disappear followed by a catastrophe. mal3p localizes normally in tip1-deleted cells and disappears from microtubule tips preceding the premature catastrophes. In contrast, tip1p requires mal3p to localize at microtubule tips. mal3p and tip1p directly interact in vitro.Conclusions: mal3p and tip1p form a system allowing microtubules to target cell ends. We propose that mal3p stimulates growth initiation and maintains growth by suppressing catastrophes. At cell ends, mal3p disappears from microtubule tips followed by a catastrophe. mal3p is involved in recruiting tip1p to microtubule tips. This becomes important when microtubules contact the cell cortex outside the cell ends because mal3p dissociates prematurely without tip1p, which is followed by a premature catastrophe.