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AKAP95 interacts with nucleoporin TPR in mitosis and is important for the spindle assembly checkpoint.

Cell Cycle. 2017 May 19;16(10):947-956. doi:10.1080/15384101.2017.1310350. Epub 2017 Apr 05
Graciela López-Soop 1 , Torunn Rønningen 1 , Agnieszka Rogala 2 , Nina Richartz 3 , Heidi Kiil Blomhoff 3 , Bernd Thiede 4 , Philippe Collas 1 , Thomas Küntziger 2
Graciela López-Soop 1 , Torunn Rønningen 1 , Agnieszka Rogala 2 , Nina Richartz 3 , Heidi Kiil Blomhoff 3 , Bernd Thiede 4 , Philippe Collas 1 , Thomas Küntziger 2
+ et al

[No authors listed]

Author information
  • 1 b Norwegian Center for Stem Cell Research, Oslo University Hospital , Oslo , Norway.
  • 2 c Department of Oral Biology, Faculty of Dentistry , University of Oslo , Oslo , Norway.
  • 3 a Department of Molecular Medicine, Faculty of Medicine , University of Oslo , Oslo , Norway.
  • 4 d Department of Biosciences, Faculty of Mathematics and Natural Sciences , University of Oslo , Oslo , Norway.

摘要


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.

KEYWORDS: mitotic arrest deficient, translocated in promoter region