MISP regulates the IQGAP1/Cdc42 complex to collectively orchestrate spindle orientation and mitotic progression.
Ontology highlight
ABSTRACT: Precise mitotic spindle orientation is essential for both cell fate and tissue organization while defects in this process are associated with tumorigenesis and other diseases. In most animal cell types, the dynein motor complex is anchored at the cell cortex and exerts pulling forces on astral microtubules to position the spindle. The actin-binding protein MISP controls spindle orientation and mitotic progression in human cells. However, the exact underlying mechanism remains to be elucidated. Here we report that MISP interacts with the multidomain scaffolding protein IQGAP1. We further show that MISP binds to the active form of Cdc42 through IQGAP1. Depletion of MISP promotes increased accumulation of IQGAP1 at the cell cortex and a decrease in its Cdc42-binding capacity leading to reduce
SUBMITTER: Vodicska B
PROVIDER: S-EPMC5910412 | biostudies-literature | 2018 Apr
REPOSITORIES: biostudies-literature
ACCESS DATA