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PrintDorothy Beckett
Professor
Personal Data
Education
- A.B., Chemistry,1980, Barnard College, Columbia University
- Ph.D., Biochemistry, 1986, Universityof Illinois, Urbana-Champaign
- 1986-1987 Postdoctoral Fellow with Dr. Robert T. Sauer Department of Biology,Massachusetts Institute of Technology
- 1986-1990, NIH Postdoctoral Fellow with Dr. Gary K. Ackers, Department of Biology, Johns Hopkins University and Dr. Robert T. Sauer, Department of Biology, Massachusetts Institute of Technology
- 1987-1990 Postdoctoral Fellow with Dr. Gary K. Ackers Department of Biology, Johns Hopkins University
Professional Experience
- 1990-1996, Assistant Professor, University of Maryland Baltimore County
- 1996-1999, Associate Professor, University of Maryland Baltimore County
- 1999-2002, Associate Professor, University of Maryland College Park
- 2002-present, Professor, University of Maryland College Park
Research Interests
Regulatory mechanisms in complex biological circuits, allostery, biophysical chemistry
Major Recognitions and Honors
- NIH Postdoctoral Fellowship, 1987-1990
- DuPont Young Professor, 1993-1996
- Secretary-elect, Biophysical Society
Significant Professional Service and Activities
NIH-NIGMS, BBCA Panel-Member 2000-2004, R32 Panel Member, October, 2005, March, 2006, March, 2007, S10 Review Panel, August, 2006, August, 2007, MFSE (ad hoc) October, 2008, NSF-Major Research
Instrumentation Panel-Member, 1997-1999, 2000 Preproposal Review Panel-Integrative Graduate Education and Research Training (IGERT) Program 1999, 2002 Ad-Hoc reviewer for individual proposals. Biophysical Society: Council: 2000-2003 (elected position), Executive Board: 2001-2003, Annual Meeting Program Committee:2000-2003, Elected Chair, Molecular Biophysics Subgroup:2001-2002, Chair, Nominations Committee: 2003-2004, Member, 2004-2005, 50th Anniversary Meeting Committee, Member: 2003-2006, Secretary of the Biophysical Society, Term-2007-2011, President, Gibbs Conference on Biothermodynamics: 2005-2006, Co-Chair (with Michael Hecht), 2010 Biopolymers Gordon Research Conference
Instrumentation Panel-Member, 1997-1999, 2000 Preproposal Review Panel-Integrative Graduate Education and Research Training (IGERT) Program 1999, 2002 Ad-Hoc reviewer for individual proposals. Biophysical Society: Council: 2000-2003 (elected position), Executive Board: 2001-2003, Annual Meeting Program Committee:2000-2003, Elected Chair, Molecular Biophysics Subgroup:2001-2002, Chair, Nominations Committee: 2003-2004, Member, 2004-2005, 50th Anniversary Meeting Committee, Member: 2003-2006, Secretary of the Biophysical Society, Term-2007-2011, President, Gibbs Conference on Biothermodynamics: 2005-2006, Co-Chair (with Michael Hecht), 2010 Biopolymers Gordon Research Conference
THE SYSTEMS
Biotin plays a critical role in metabolism in all organisms and elaborate systems have evolved to regulate its homeostasis. We study the E. coli and the human systems.
Humans do not synthesize biotin and, as illustrated in the Mammalian Biotin Cycle on the right, it is transported into cells via a transporter, linked to the five biotin-dependent carboxylases, and recycled after degradation of the carboxylases. We are currently studying regulation of biotin distribution to the carboxylases. Post-translational biotin addition to these carboxylases is catalyzed by holocarboxylase synthetase (HCS) and measurements of the kinetics of biotin transfer to the five carboxylases indicates a 100-fold range in the the rates. This suggests a mechanism of biotin distribution that is regulated by the combined intrinsic transfer rates and relative concentrations of the carboxylases. The regulation could potentially influence important metabolic processes including gluconeogenesis, amino acid catabolism and fatty acid synthesis and oxidation.
Biotin plays a critical role in metabolism in all organisms and elaborate systems have evolved to regulate its homeostasis. We study the E. coli and the human systems.
I. The E. coli Biotin Regulatory System 
This biological circuit, outlined in the figure to the right, functions both in funneling the vitamin, biotin, into fatty acid synthesis and in regulating its synthesis. The central protein of the circuit, BirA, catalyzes covalent attachment of biotin to BCCP, a subunit of the biotin-dependent enzyme, acetyl CoA carboxylase. BirA also binds sequence-specifically to the transcription operator of the biotin biosynthetic operon to repress transcription initiation, thereby regulating intracellular biotin concentration. Our goal is to determine the rules that govern functional switching of BirA from enzyme to transcription repressor. Combined biochemical and biophysical tools are used in this effort.
II. The Human Biotin Cycle
Humans do not synthesize biotin and, as illustrated in the Mammalian Biotin Cycle on the right, it is transported into cells via a transporter, linked to the five biotin-dependent carboxylases, and recycled after degradation of the carboxylases. We are currently studying regulation of biotin distribution to the carboxylases. Post-translational biotin addition to these carboxylases is catalyzed by holocarboxylase synthetase (HCS) and measurements of the kinetics of biotin transfer to the five carboxylases indicates a 100-fold range in the the rates. This suggests a mechanism of biotin distribution that is regulated by the combined intrinsic transfer rates and relative concentrations of the carboxylases. The regulation could potentially influence important metabolic processes including gluconeogenesis, amino acid catabolism and fatty acid synthesis and oxidation.
