Sakuno, T., Tanaka, K., Hauf, S. & Watanabe, Y. Repositioning of aurora B promoted by chiasmata ensures sister chromatid mono-orientation in meiosis I.
Frequent mono-orientation in mps1-as1 suggests that one or some of these steps are defective.
Our experiment also demonstrates that Rec8-cohesin is necessary for sister kinetochore mono-orientation in oocytes.
Rather, we suspect that the abnormal spindle is the outcome of extensive centromere mono-orientation in mps1-as1 cells.
Consequently, merotelic attachment might not be possible, which would explain the unperturbed mono-orientation in Ipl1-depleted cells (Monje-Casas et al, 2007) despite the otherwise similar function of Ipl1 and Ark1.
Since Moa1 localization is intact in either sgo2Δ or bub1Δ cells (data not shown), it is reasonable to assume that perturbation of mono-orientation in these cells may originate from the reduced Ark1 activity at centromeres.
Thus, the mono-orientation defect caused by the reduction of Ark1 is likely different from the one caused by the absence of Moa1 or Rec8, suggesting that Ark1 and Moa1/Rec8 influence sister kinetochore mono-orientation in meiosis-I through distinct mechanisms.
Little is known about the molecular events that occur during conversion from chromosome mono-orientation to bi-orientation in any organism.
When contemplating the reason for the mono-orientation defect in ark1 s.o.o
The mono-orientation defect in ark1 s.o. cells is less pronounced, and Moa1- or Rec8-localization is not disrupted when Ark1 is depleted.
Based on the results described above, we hypothesized that the mono-orientation defect in sgo2Δ cells originates from the inability to correct merotelic attachment of paired sister kinetochores, like in ark1 s.o.o
