Our research focuses on understanding the molecular mechanisms regulating DNA repair, chromosome segregation and cell cycle progression. Our lab studies the importance of Structural Maintenance of Chromosomes (SMC) complexes and cell cycle kinases, particularly Polo-like (PLK) kinases and Aurora kinases. We use mouse as a model organism to study consequences of gene mutation and chromosome missegregation, which give rise to physical and cognitive developmental defects, infertility and cancer predisposition. We also use mouse and human pluripotent stem cells to help define the function of these proteins within essential molecular pathways of the cell.
Hwang G, O’Brien M, Sun F, Eppig J, Handel MA, Jordan PW. SMC5/6 is required for the formation of segregation-competent bivalent chromosomes during meiosis I in mouse oocytes. Development. 2017 PMID: 28302748.
Pryzhkova MV, Jordan PW. Conditional mutation of Smc5 in mouse embryonic stem cells perturbs condensin localization and mitotic progression. J Cell Sci. 2016 PMID: 26919979.
Hopkins J, Hwang G, Jacob J, Sapp N, Bedigian R, Oka K, Overbeek P, Murray S, Jordan PW. Meiosis-specific cohesin component, Stag3 is essential for maintaining centromere chromatid cohesion, and required for DNA repair and synapsis between homologous chromosomes. PLoS Genet. 2014 PMID: 24992337.
Jordan PW, Karppinen J, Handel MA. Polo-like kinase is required for synaptonemal complex disassembly and phosphorylation in mouse spermatocytes. J Cell Sci. 2012 PMID: 22854038.
Jordan P, Copsey A, Newnham L, Kolar E, Lichten M, Hoffmann E. Ipl1/Aurora B kinase coordinates synaptonemal complex disassembly with cell cycle progression and crossover formation in budding yeast meiosis. Genes Dev. 2009 PMID: 19759266.