Although its function in interphase is unknown, transient inhibition of Aurora B kinase activity in interphase gives rise to segregation defects in anaphase, suggesting that already before mitosis Aurora B may regulate proper kinetochore formation or function (Emanuele et al. 2008; Hayashi-Takanaka et al. 2009).
Efficient chromosome segregation during mitosis relies on the coordinated activity of molecular motors with proteins that regulate kinetochore attachments to dynamic spindle microtubules [1].
Tension at kinetochores, brought about by bipolar association of condensin-tethered chromosomes in the mitotic spindle, originally was proposed by Nicklas and Koch (Nicklas and Koch 1969) to regulate kinetochore microtubule dynamics.
Together, these results are consistent with the idea that PP1 acts on Aurora B substrates to regulate kinetochore microtubule dynamics and SAC silencing.
This amounts to a ∼1.6 fold increase when compared to metaphase without NDGA treatment, and again suggests that inter-kinetochore tension may regulate hZW10 transport off kinetochores.
In addition, the possibility that the kinetochore itself may regulate this rate is also intriguing and worth testing (see Box 1 for a thorough discussion).
We show for the first time that MK2 may regulate bipolar spindle stability, microtubule-kinetochore attachments and chromosome segregation to participate in meiotic cell cycle regulation.
However, a significant fraction of GFP-5R-expressing cells displayed persistent kinetochore localization of BubR1 at anaphase and telophase stages, strongly suggesting that Kif18A sumoylation may regulate the removal of BubR1 from the kinetochores and compromise its inactivation.
Given that Mps1 and Ipl1 kinases play similar roles in promoting sister-kinetochore bi-orientation [3, 6, 24], we addressed whether one may regulate function of the other.
Alternatively, FruM may regulate dopamine neuronal activities.
