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HAUS6的钙调蛋白同源结构域在锚定augmin以促进微管分支中的保守功能。

Conserved function of the HAUS6 calponin homology domain in anchoring augmin for microtubule branching.

作者信息

Würtz Martin, Tonon Giulia, Vermeulen Bram J A, Zezlina Maja, Gao Qi, Neuner Annett, Seidl Angelika, König Melanie, Harkenthal Maximilian, Eustermann Sebastian, Erhardt Sylvia, Lolicato Fabio, Schiebel Elmar, Pfeffer Stefan

机构信息

Zentrum für Molekulare Biologie der Universität Heidelberg (ZMBH), Heidelberg, Germany.

European Molecular Biology Laboratory (EMBL), Heidelberg, Germany.

出版信息

Nat Commun. 2025 Aug 22;16(1):7845. doi: 10.1038/s41467-025-63165-z.

Abstract

Branching microtubule nucleation is a key mechanism for mitotic and meiotic spindle assembly and requires the hetero-octameric augmin complex. Augmin recruits the major microtubule nucleator, the γ-tubulin ring complex, to pre-existing microtubules to direct the formation of new microtubules in a defined orientation. Although recent structural work has provided key insights into the structural organization of augmin, molecular details of its interaction with microtubules remain elusive. Here, we identify the minimal conserved microtubule-binding unit of augmin across species and demonstrate that stable microtubule anchoring is predominantly mediated via the calponin homology (CH) domain in Dgt6/HAUS6. Comparative sequence and functional analyses in vitro and in vivo reveal a highly conserved functional role of the HAUS6 CH domain in microtubule binding. Using cryo-electron microscopy and molecular dynamics simulations in combination with AlphaFold structure predictions, we show that the D. melanogaster Dgt6/HAUS6 CH domain binds microtubules at the inter-protofilament groove between two adjacent β-tubulin subunits and thereby orients augmin on microtubules. Altogether, our findings reveal how augmin binds microtubules to pre-determine the branching angle during microtubule nucleation and facilitate the rapid assembly of complex microtubule networks.

摘要

分支微管成核是有丝分裂和减数分裂纺锤体组装的关键机制,需要异源八聚体augmin复合物参与。Augmin将主要的微管成核因子γ-微管蛋白环复合物招募到已有的微管上,以特定方向指导新微管的形成。尽管最近的结构研究为augmin的结构组织提供了关键见解,但其与微管相互作用的分子细节仍不清楚。在这里,我们确定了跨物种的augmin最小保守微管结合单元,并证明稳定的微管锚定主要通过Dgt6/HAUS6中的钙调蛋白同源(CH)结构域介导。体外和体内的比较序列及功能分析揭示了HAUS6 CH结构域在微管结合中具有高度保守的功能作用。结合冷冻电子显微镜、分子动力学模拟以及AlphaFold结构预测,我们发现果蝇Dgt6/HAUS6 CH结构域在两个相邻β-微管蛋白亚基之间的原丝间凹槽处结合微管,从而在微管上确定augmin的方向。总之,我们的研究结果揭示了augmin如何结合微管以在微管成核过程中预先确定分支角度,并促进复杂微管网络的快速组装。

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