Cell division is a fundamental process forming the basis for life itself. Each time a cell divides, it makes a complete copy of its entire genome and segregates this genome such that both daughter cells receive all the genetic information required for further growth and development.
Errors in the distribution of chromosomes during mitosis lead to the production of cells with an abnormal chromosome content, which in early development lead to lethal growth defects and may later contribute to the development of cancer.
The Holland Lab is interested in the molecular mechanisms that control accurate chromosome distribution and the role that mitotic errors play in human health and disease.
The lab utilizes a combination of chemical biology, biochemistry, cell biology and genetically engineered mice to study pathways involved in mitosis and their effect on cell and organism physiology.
A major focus of the group is to develop cell and animal-based models to study the role of cell division defects in genome instability and tumorigenesis.
Lab Website: Holland Lab
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Holland AJ*, Fachinetti D, Zhu Q, Bauer M, Verma IM, Nigg EA, Cleveland DW. The autoregulated instability of Polo-like kinase 4 limits centrosome duplication to once per cell cycle. Genes Dev. 2012. PMCID: PMC3533073
Moyer TC, Clutario KM, Lambrus BG, Daggubati V, Holland AJ*. Binding of STIL to Plk4 activates kinase activity to promote centriole assembly. J Cell Biol. 2015. PMCID: PMC4477857
Lambrus BG, Uetake Y, Clutario KM, Daggubati V, Snyder M, Sluder G, Holland AJ*. p53 protects against genome instability following centriole duplication failure. J Cell Biol. 2015. PMCID: PMC4494000
Lambrus BG, Daggubati V, Uetake Y, Scott PM, Clutario KM, Sluder G, Holland AJ*. A USP28-53BP1-p53-p21 signaling axis arrests growth after centrosome loss or prolonged mitosis. J Cell Biol. 2016 Jul 18;214(2):143-53. PMCID: PMC4949452
Kim Y*, Holland AJ*, Lan W, Cleveland DW. Aurora kinases and protein phosphatase 1 mediate chromosome congression through regulation of CENP-E. Cell. 2010 Aug 6;142(3):444-55. *equal contribution. PMCID: PMC2921712