Michael P. Kladde

Michael P. Kladde, Ph.D.
Associate Professor

PH:  352-273-8142
FX:  352-273-8299
Email:  kladde@ufl.edu

University of Florida
Dept. of Biochemistry & Molecular Biology
2033 Mowry Road
Gainesville, FL  32610





Associate Professor Mike Kladde earned his Ph.D. degree in Cellular and Molecular Biology with Dr. Jack Gorski at the University of Wisconsin-Madison in 1991 on estrogenic regulation of gene expression. He then pursued postdoctoral work on chromatin structure and function in the laboratory of Dr. Robert T. Simpson at the National Institutes of Health and then at The Pennsylvania State University. Dr. Kladde took a position at Texas A&M University in 1998 and rose to the rank of Associate Professor continuing his studies on activation of gene expression in the context of chromatin. He joined the Department of Biochemistry and Molecular Biology at UF in 2007. Dr. Kladde has served on NIH study section and as a reviewer for NSF and numerous journals in the field.


The packaging of DNA into nucleosomes, the repeating unit of chromatin comprised of histones, essentially regulates all biological functions of DNA in eukaryotes. One emphasis of the lab is on transcriptional activation, specifically, studying how chromatin-mediated repression is overcome through histone modifications (for example, acetylation) and the disassembly of nucleosomes, a process termed chromatin remodeling. These studies focus on induction of the PHO5 promoter in response to phosphate limitation, a proven model system for investigating chromatin remodeling in the budding yeast S. cerevisiae. Yeast offers many experimental advantages, including ease in biochemical, genetic, and molecular approaches. We have also identified a novel role for cell cycle regulators in PHO5 transcription and are currently determining their regulatory functions. Another area of investigation concerns the role of epigenetic or post-replicative methylation of DNA in tumor progression. In a recent collaboration, we have discovered increased DNA methylation of a novel mammalian tumor suppressor gene that is associated with elevated invasiveness of breast cancer. Future studies will examine mechanisms of epigenetic silencing of this tumor suppressor in human breast cancer lines and patient tumor tissue. Both areas of study take advantage of our powerful population and single-molecule strategies (MAP and MAP-IT, respectively) for probing chromatin structure with DNA methyltransferases

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