Trim9 and Klp61F promote polymerization of new dendritic microtubules along parallel microtubules
Trim9 and Klp61F promote polymerization of new dendritic microtubules along parallel microtubules
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DOI：
10.1242/jcs.258437
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发表时间：
2021-06-01
影响因子：
4
通讯作者：
Rolls, Melissa M.
中科院分区：
文献类型：
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作者：
Feng, Chengye;Cleary, Joseph M.;Rolls, Melissa M.
轴突和树突通过微管极性来区分。在果蝇中，树突以负端微管为主，而轴突则含有正端微管。树突中的局部成核在两个方向上产生微管。为了理解为什么树突成核不会破坏极性，我们使用实时成像来分析分支点处生成的微管的命运。我们发现，根据方向，它们离开分支的成功率不同：正确方向的负端出微管成功离开分支的几率是方向错误的微管的两倍。更大的成功依赖于平行方向的其他微管。从候选筛选中，我们确定 Trim9 和驱动蛋白 5 (Klp61F) 是促进新微管生长的机制。在 S2 细胞中，Eb1 将 Trim9 招募到微管中。 Klp61F 在体外和体内促进微管生长，并且可以在 S2 细胞中招募 Trim9。总之，数据表明 Trim9 和 kinesin-5 在微管正端共同作用，帮助与预先存在的微管平行的聚合微管抵抗灾难。
Axons and dendrites are distinguished by microtubule polarity. In Drosophila, dendrites are dominated by minus-end-out microtubules, whereas axons contain plus-end-out microtubules. Local nucleation in dendrites generates microtubules in both orientations. To understand why dendritic nucleation does not disrupt polarity, we used live imaging to analyze the fate of microtubules generated at branch points. We found that they had different rates of success exiting the branch based on orientation: correctly oriented minus-end-out microtubules succeeded in leaving about twice as often as incorrectly oriented microtubules. Increased success relied on other microtubules in a parallel orientation. From a candidate screen, we identified Trim9 and kinesin-5 (Klp61F) as machinery that promoted growth of new microtubules. In S2 cells, Eb1 recruited Trim9 to microtubules. Klp61F promoted microtubule growth in vitro and in vivo, and could recruit Trim9 in S2 cells. In summary, the data argue that Trim9 and kinesin-5 act together at microtubule plus ends to help polymerizing microtubules parallel to pre-existing ones resist catastrophe.