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E3 连接酶TRIM37对微管组织中心的中尺度调控

Mesoscale regulation of microtubule-organizing centers by the E3 ligase TRIM37.

作者信息

Yeow Zhong Y, Sarju Sonia, Chang Fang-Chi, Xu Lance Y, van Breugel Mark, Holland Andrew J

机构信息

Department of Molecular Biology and Genetics, Johns Hopkins University School of Medicine, Baltimore, MD, USA.

School of Biological and Behavioural Sciences, Queen Mary University of London, London, UK.

出版信息

Nat Struct Mol Biol. 2025 May 25. doi: 10.1038/s41594-025-01540-6.

Abstract

Centrosomes ensure accurate chromosome segregation during cell division. Although the regulation of centrosome number is well established, less is known about the suppression of noncentrosomal microtubule-organizing centers (ncMTOCs). The E3 ligase TRIM37, implicated in Mulibrey nanism and 17q23-amplified cancers, has emerged as a key regulator of both centrosomes and ncMTOCs. Yet, the mechanism by which TRIM37 achieves enzymatic activation to target these mesoscale structures had thus far remained unknown. Here we elucidate the activation process of TRIM37, unveiling a process that initiates with TRAF domain-directed substrate recognition followed by B-box domain-mediated oligomerization and culminates in RING domain dimerization. Using optogenetics, we demonstrate that the E3 activity of TRIM37 is directly coupled to the assembly state of its substrates, being activated only when centrosomal proteins cluster into higher-order assemblies resembling MTOCs. This regulatory framework provides a mechanistic basis for understanding TRIM37-driven pathologies and echoes the restriction of the human immunodeficiency virus capsid by TRIM5, thus unveiling a conserved activation blueprint among TRIM proteins to control turnover of complexes assembled at the mesoscale level.

摘要

中心体确保细胞分裂过程中染色体的准确分离。尽管中心体数量的调控机制已得到充分确立,但对于非中心体微管组织中心(ncMTOCs)的抑制作用了解较少。E3连接酶TRIM37与穆利布雷侏儒症和17q23扩增的癌症有关,已成为中心体和ncMTOCs的关键调节因子。然而,TRIM37实现酶促激活以靶向这些中尺度结构的机制迄今为止仍不清楚。在这里,我们阐明了TRIM37的激活过程,揭示了一个始于TRAF结构域导向的底物识别、接着是B-box结构域介导的寡聚化、并最终以RING结构域二聚化告终的过程。利用光遗传学,我们证明TRIM37的E3活性直接与其底物的组装状态相关联,仅当中心体蛋白聚集成类似MTOCs的高阶组装体时才被激活。这种调控框架为理解TRIM37驱动的病理学提供了机制基础,并与TRIM5对人类免疫缺陷病毒衣壳的限制相呼应,从而揭示了TRIM蛋白之间保守的激活蓝图,以控制在中尺度水平组装的复合物的周转。

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