ArticleCell cycle (Georgetown, Tex.)2017
AKAP95 interacts with nucleoporin TPR in mitosis and is important for the spindle assembly checkpoint.
Article in Cell cycle (Georgetown, Tex.), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed.
- The autophagy protein Ambra1 regulates gene expression by supporting novel transcriptional complexes.The Journal of biological chemistry · 2020Article
- The complex activities of the SET1/MLL complex core subunits in development and disease.Biochimica et biophysica acta. Gene regulatory mechanisms · 2020Review
- Proximity Labeling Techniques to Study Chromatin.Frontiers in genetics · 2020Review
- Specific inhibition of DPY30 activity by ASH2L-derived peptides suppresses blood cancer cell growth.Experimental cell research · 2019Article
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8 authors.
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Abstract
Faithful chromosome segregation during mitosis relies on a proofreading mechanism that monitors proper kinetochore-microtubule attachments. The spindle assembly checkpoint (SAC) is based on the concerted action of numerous components that maintain a repressive signal inhibiting transition into anaphase until all chromosomes are attached. Here we show that A-Kinase Anchoring Protein 95 (AKAP95) is necessary for proper SAC function. AKAP95-depleted HeLa cells show micronuclei formed from lagging chromosomes at mitosis. Using a BioID proximity-based proteomic screen, we identify the nuclear pore complex protein TPR as a novel AKAP95 binding partner. We show interaction between AKAP95 and TPR in mitosis, and an AKAP95-dependent enrichment of TPR in the spindle microtubule area in metaphase, then later in the spindle midzone area. AKAP95-depleted cells display faster prometaphase to anaphase transition, escape from nocodazole-induced mitotic arrest and show a partial delocalization from kinetochores of the SAC component MAD1. Our results demonstrate an involvement of AKAP95 in proper SAC function likely through its interaction with TPR.
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