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Haploid gametes (sperm and eggs) are generated by meiosis and are essential for sexual reproduction. In females, meiosis is highly error-prone as ~5-20% of a young, healthy woman’s eggs contain an abnormal number of chromosomes (aneuploid). Aneuploidy is the leading cause of infertility, miscarriage and, in the case of live birth, developmental disorders such as Down Syndrome. Little is known, however, about how meiosis in females is regulated and why it is so prone to chromosome segregation mistakes. Research in our group uses the mouse oocyte model to understand how signal transduction networks, specifically at the level of protein kinases and protein phosphatases, regulate female meiosis.
Balboula, AZ, and Schindler, K. 2014. Selective Disruption of Aurora C Kinase Reveals Distinct Functions From Aurora B Kinase During Meiosis in Mouse Oocytes. Plos Genetics.10(2):e1004194.
Balboula, AZ, Stein, P, Schultz, RM and Schindler, K. 2014. Knockdown of RBBP7 unveils a requirement of histone deacetylation for CPC function in mouse oocytes. Cell Cycle. 13(4):600-11.
Oh JS, Susor A, Schindler K, Schultz RM, Conti M. 2013. Cdc25A activity is required for the metaphase II arrest in mouse oocytes. Journal of Cell Science. 126(Pt 5): 1081-5.
Schindler K*, Davydenko O*, Fram B, Lampson MA, Schultz RM. (2012) Maternally-recruited Aurora C kinase is more stable than Aurora B to support mouse oocyte maturation and early development. PNAS 109(33): E2215-22.