NuSAP Safeguards Centriole Integrity to Mediate CEP57‐CEP152 Torus Recruitment for Proper Engagement
Precise centrosome regulation is crucial for faithful cell division, yet how microtubule-associated proteins (MAPs) contribute to centrosome integrity remains poorly understood. Here, we uncover a novel localization of NuSAP-a RanGTP-regulated MAP-on centrioles using super-resolution microscopy. NuSAP depletion disrupts centriole tubulin architecture, triggering premature centriole disengagement, compromising pericentriolar material (PCM) cohesion, and disrupting the spatial organization of the CEP57-CEP63-CEP152 torus assembly. Using TurboID-based proteomics and biochemical assays, we identify CEP57 as a direct interactor of NuSAP. We further demonstrate that NuSAP is essential for the initial recruitment of the CEP57-CEP63-CEP152 complex to the proximal end of procentrioles. Based on these findings, we propose a novel two-step model of torus complex recruitment, in which NuSAP-dependent stabilization of centriole tubulin is required for early CEP57 loading. This discovery not only resolves a longstanding gap in our understanding of how MAP-mediated tubulin stabilization contributes to centrosome organization but also provides a mechanistic framework for the hierarchical recruitment of the centriole torus complex.
Authors
- Karen Crasta (ORCID: https://orcid.org/0000-0001-9849-6080)
- Zemin Jiang
- Shiyu Zhang (ORCID: https://orcid.org/0009-0009-7047-1872)
- Minghao Wang
- Qiaoyun Yang
- Chennianci Zhu
- Lih‐Wen Deng
- Hong Zheng
- Yih‐Cherng Liou
Institutions
- Army Medical University (CN)
- National University of Singapore (SG)
- National University Cancer Institute, Singapore (SG)
- Xinqiao Hospital (CN)
- Southwest Hospital (CN)
- National Cancer Centre Singapore (SG)
- National University Health System (SG)
Publication Details
- Journal
- Advanced Science
- Published
- 2026-01-30
- DOI
- https://doi.org/10.1002/advs.202515192
- Primary Topic
- Microtubule and mitosis dynamics
- Type
- article
- Field-Weighted Citation Impact
- 0.00