AI Article Synopsis
- Proper assembly of kinetochores (KTs) during mitosis is crucial for proper spindle attachment and accumulation of checkpoint components.
- Tex14, a protein linked to midbody function, is recruited to KTs by Plk1 in a Cdk1-dependent manner, and its exclusion leads to various chromosome stability issues.
- Phosphorylation of Tex14 by Plk1 during metaphase causes its degradation, and inhibiting this process results in retention at KTs, delaying the transition from metaphase to anaphase and causing chromosome segregation problems.
Article Abstract
Proper assembly of kinetochores (KTs) during mitosis is required for bipolar attachment of spindle microtubules (MTs) and the accumulation of spindle assembly checkpoint (SAC) components. Here we show that testis-expressed protein 14 (Tex14), which has been implicated in midbody function, is recruited to KTs by Plk1 in a Cdk1-dependent manner during early mitosis. Exclusion of Tex14 from kinetochores results in an inability to efficiently localize outer KT components, impaired KT-MT attachment, chromosome congression defects, and whole-chromosome instability. In addition, we demonstrate that phosphorylation of Tex14 by Plk1 during metaphase promotes APC(Cdc20)-mediated Tex14 degradation. Inhibition of this phosphorylation event causes retention of Tex14 at KTs and results in delayed metaphase-to-anaphase transition and chromosome segregation defects. Our findings identify Tex14 as an important mediator of KT structure and function and the fidelity of chromosome separation.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3302152 | PMC |
| http://dx.doi.org/10.1016/j.molcel.2012.01.013 | DOI Listing |
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