In our discussion we mainly focused on the meiotic/mitotic spindle connections of the identified by us proteins.
Both the proper chromosome-spindle connection and SAC are regulated by a number of crucial phosphorylation events catalyzed by protein kinases including Aurora B, Mps1 and Bub1 (Funabiki and Wynne, 2013; Musacchio, 2015).
A) For example, with respect to the physiological role of outer-kinetochore disassembly during prophase, the authors' interpretation is that this process is redundant with suppression of cyclins in preventing premature kinetochore-spindle connections.
Failure in bi-orientation with inactive Mps1 is not due to a lack of kinetochore-spindle pole connections by microtubules, but due to a defect in properly orienting the connections.
Taken together, failure in bi-orientation upon Mps1 inactivation is not due to absence or loss of kinetochore-spindle pole connections but is due to defects in achieving proper orientation of these connections.
Mps1 promotes re-orientation of kinetochore-spindle pole connections and eliminates those that do not generate tension between sister kinetochores.
This re-orientation is facilitated by Aurora B kinase (Ipl1 in budding yeast), which eliminates kinetochore-spindle pole connections that do not generate tension [3 6].
This error correction stems from stabilization of kinetochore-spindle pole connections by tension, arising from bi-orientation but not syntelic attachment [6, 23].
It remains completely unproven whether the physiological role of outer kinetochore disassembly in prophase I is to prevent premature spindle-kinetochore connections.
If sister kinetochores attach to microtubules from the same pole (syntelic attachment), the kinetochore-spindle pole connections must be re-oriented to be converted to proper bi-orientation [1, 2].
These data suggest that the Mps1 kinase does indeed have an important role in eliminating kinetochore-spindle pole connections when they cannot come under tension normally generated by bi-orientation.
