Linking centromere stretch to SAC signaling in mammalian oocytes with insights from modified kinetochore model
Abstract
The spindle assembly checkpoint (SAC) monitors kinetochore-microtubule interactions to ensure accurate chromosome segregation. In mitosis, investigation of its silencing at anaphase centers on whether attachment or tension is the key signal, while in meiosis for mammalian oocytes it remains unclear whether centromere stretching contributes to SAC deactivation, because in this reductional division sister chromatids co-segregate during meiosis I. While previous studies have linked bivalent tension to SAC control in oocytes, this measurement cannot be directly equated with mitotic chromatin stretching. Here, by tagging the N-terminus of NDC80/HEC1, we developed a mouse oocyte model that features stable microtubule attachments, yet exhibits persistent SAC signaling at metaphase I. Our comprehensive analysis reveals a strong correlation between centromere stretching and SAC signaling. Furthermore, high-resolution live imaging demonstrates that these modified kinetochores impair their oscillatory movements, a process vital for error correction, while chromosome congression remains largely unaffected. Collectively, our data suggest that stable microtubule attachment alone is insufficient to silence SAC in mammalian oocytes; instead, centromere stretching may serve as a critical signal to deactivate the checkpoint. These findings underscore the adaptability of core cell-cycle surveillance pathways.
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BibTeX
@article{yun2026linking,
title = {{Linking centromere stretch to SAC signaling in mammalian oocytes with insights from modified kinetochore model}},
author = {Yan Yun and Simon I. R. Lane and Ziyang Guo and Zhixiang Zheng and Wenfeng Cai and Janet E. Holt and Keith T. Jones},
journal = {Communications Biology},
year = {2026},
month = oct,
doi = {10.1038/s42003-026-11126-7},
url = {https://www.nature.com/articles/s42003-026-11126-7},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Linking centromere stretch to SAC signaling in mammalian oocytes with insights from modified kinetochore model
AU - Yan Yun
AU - Simon I. R. Lane
AU - Ziyang Guo
AU - Zhixiang Zheng
AU - Wenfeng Cai
AU - Janet E. Holt
AU - Keith T. Jones
PY - 2026
DA - 2026/10/11
JO - Communications Biology
DO - 10.1038/s42003-026-11126-7
UR - https://www.nature.com/articles/s42003-026-11126-7
AB - The spindle assembly checkpoint (SAC) monitors kinetochore-microtubule interactions to ensure accurate chromosome segregation. In mitosis, investigation of its silencing at anaphase centers on whether attachment or tension is the key signal, while in meiosis for mammalian oocytes it remains unclear whether centromere stretching contributes to SAC deactivation, because in this reductional division sister chromatids co-segregate during meiosis I. While previous studies have linked bivalent tension to SAC control in oocytes, this measurement cannot be directly equated with mitotic chromatin stretching. Here, by tagging the N-terminus of NDC80/HEC1, we developed a mouse oocyte model that features stable microtubule attachments, yet exhibits persistent SAC signaling at metaphase I. Our comprehensive analysis reveals a strong correlation between centromere stretching and SAC signaling. Furthermore, high-resolution live imaging demonstrates that these modified kinetochores impair their oscillatory movements, a process vital for error correction, while chromosome congression remains largely unaffected. Collectively, our data suggest that stable microtubule attachment alone is insufficient to silence SAC in mammalian oocytes; instead, centromere stretching may serve as a critical signal to deactivate the checkpoint. These findings underscore the adaptability of core cell-cycle surveillance pathways.
SN - 2399-3642
ER -