Successful cell division requires that chromosomes attach to opposite poles of the mitotic spindle (bi-orientation). Aurora B kinase regulates chromosome-spindle attachments by phosphorylating kinetochore substrates that bind microtubules. Centromere tension stabilizes bi-oriented attachments, but how physical forces are translated into signaling at individual centromeres is unknown. Using fluorescence resonance energy transfer-based biosensors to measure localized phosphorylation dynamics in living cells, we found that phosphorylation of an Aurora B substrate at the kinetochore depended on its distance from the kinase at the inner centromere. Furthermore, repositioning Aurora B closer to the kinetochore prevented stabilization of bi-oriented attachments and activated the spindle checkpoint. Thus, centromere tension can be sensed by increased spatial separation of Aurora B from kinetochore substrates, which reduces phosphorylation and stabilizes kinetochore microtubules.
Identification of a subdomain of CENP-B that is necessary and sufficient for localization to the human centromere
Chromosomal proteins and cytokinesis: patterns of cleavage furrow formation and inner centromere protein positioning in mitotic heterokaryons and mid-anaphase cells
Probing spindle assembly mechanisms with monastrol, a small molecule inhibitor of the mitotic kinesin, Eg5
INCENP binds the Aurora-related kinase AIRK2 and is required to target it to chromosomes, the central spindle and cleavage furrow
The budding yeast protein kinase Ipl1/Aurora allows the absence of tension to activate the spindle checkpoint
CENP-A is phosphorylated by Aurora B kinase and plays an unexpected role in completion of cytokinesis
Evidence that the Ipl1-Sli15 (Aurora kinase-INCENP) complex promotes chromosome bi-orientation by altering kinetochore-spindle pole connections
The small molecule Hesperadin reveals a role for Aurora B in correcting kinetochore-microtubule attachment and in maintaining the spindle assembly checkpoint
Aurora B couples chromosome alignment with anaphase by targeting BubR1, Mad2, and Cenp-E to kinetochores
Phosphoregulation and depolymerization-driven movement of the Dam1 complex do not require ring formation
Implications for kinetochore-microtubule attachment from the structure of an engineered Ndc80 complex
Family matters: structural and functional conservation of centromere-associated proteins from yeast to humans
Constitutive Mad1 targeting to kinetochores uncouples checkpoint signalling from chromosome biorientation
Formation of stable attachments between kinetochores and microtubules depends on the B56-PP2A phosphatase
Aurora B potentiates Mps1 activation to ensure rapid checkpoint establishment at the onset of mitosis
CCAAT/enhancer-binding protein delta mediates tumor necrosis factor alpha-induced Aurora kinase C transcription and promotes genomic instability.
KNL1 facilitates phosphorylation of outer kinetochore proteins by promoting Aurora B kinase activity
MCAK is present at centromeres, midspindle and chiasmata and involved in silencing of the spindle assembly checkpoint in mammalian oocytes
Microtubule plus-ends within a mitotic cell are 'moving platforms' with anchoring, signalling and force-coupling roles
BRK1, a Bub1-related kinase, is essential for generating proper tension between homologous kinetochores at metaphase I of rice meiosis
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