<i>Bcl2l10</i>, a new <i>Tpx2</i> binding partner, is a master regulator of <i>Aurora kinase A</i> in mouse oocytes

Previously, we demonstrated that <i>Bcl-2-like 10</i> (<i>Bcl2l10</i>) is associated with meiotic spindle assembly and that the gene that is most strongly down-regulated by <i>Bcl2l10</i> RNAi is <i>targeting protein for Xklp2</i> (<i>Tpx2</i>). <i>Tpx2</i> is a well-known cofactor that controls the activity and localization of <i>Aurora kinase A</i> (<i>Aurka</i>) during mitotic spindle assembly. Therefore, this study was conducted (1) to identify the associations among <i>Bcl2l10</i>, <i>Tpx2</i>, and <i>Aurka</i> and (2) to understand how <i>Bcl2l10</i> regulates meiotic spindle assembly in mouse oocytes. Bcl2l10, Tpx2, and Aurka co-localized on the meiotic spindles, and Bcl2l10 was present in the same complex with Tpx2. Tpx2 and Aurka expression decreased whereas phospho-Aurka increased in <i>Bcl2l10</i> RNAi-treated oocytes. Counterbalancing changes in the levels of these 2 activators, Tpx2 and phospho-Aurka, resulted in decreased <i>Aurka</i> catalytic activity after <i>Bcl2l10</i> RNAi treatment. <i>Bcl2l10</i> RNAi decreased the expression of microtubule organizing center (MTOC)-related proteins, disturbed MTOC formation and disrupted meiotic spindle assembly. Our data demonstrate that <i>Bcl2l10</i> is a binding partner of <i>Tpx2</i> and a new regulator of the complex controlling the organization of microtubules and MTOC biogenesis in meiotic spindle assembly. The discovery of <i>Bcl2l10</i> as a new effector of <i>Aurka</i> suggests that <i>Bcl2l10</i> may have diverse functions in mitotic cells.