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. Author manuscript; available in PMC: 2018 May 1.
Published in final edited form as: Trends Genet. 2017 Mar 27;33(5):349–363. doi: 10.1016/j.tig.2017.03.005

Figure 3. Hypothesized mechanism of AURKB-CPC and AURKC-CPC spatial distribution to explain separation of function in germ cells.

Figure 3

a) Schematic representation of hypothesized CPC sub-populations in mouse oocytes on MI bivalents. b) Survivin recognition of phosphorylated histone 3 at threonine 3 (H3pT3) drives AURKC-CPC to the interchromatid axis (ICA) and centromeres. This CPC subpopulation is responsible for error correction in meiosis I via destabilization of erroneous kinetochore-microtubule (K-MT) attachments and regulating chromosome condensation. c) Hypothesized Borealin dimerization drives AURKB/C-CPC localization to kinetochores. This CPC sub-populations functions remain unknown and may require AURKB and/or AURKC.