Jon M. Kaguni
Professor
- B.S. 1974, University of Notre Dame
- Ph.D. 1980, University of California, Los Angeles
- NIH Predoctoral Fellow, 1974-79, University of California, Los Angeles
- Damon Runyon-Walter Winchell Research Fellow, 1980-82, Stanford University School of Medicine
- MSU Teacher-Scholar Award, 1991
322 Biochemistry Building
Michigan State University
East Lansing, MI 48824-1319
Office: 517-353-6721
Lab: 517-432-3153
FAX: 517-353-9334
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Jon M. Kaguni Research Interests
A model has been proposed involving the DnaA-mediated oriented binding of DnaB helicase at the step of initiation so that it can function properly as a DNA helicase. Additional domains are involved in DNA binding, ATP binding, and in replication of pSC101. The latter is a plasmid of E. coli that requires DnaA protein for its replication. Other studies indicate that DnaA protein binds to four sites in the E. coli chromosomal origin in an ordered and sequential manner. Binding of DnaA protein to the last site, DnaA box R3, is critical in observing replication from the chromosomal origin both in vivo and in vitro. This event may be a key regulatory step in the initiation process. Finally, we have characterized biochemically a mutant form of DnaA protein with a substitution at alanine 184 with valine. Whereas wild type DnaA protein binds ATP with high affinity, this mutant protein binds ATP weakly, and requires activation by DnaK and GrpE heat shock proteins to observe ATP binding and replication activity. The impaired ability of DnaA protein to bind ATP results in a defect in the proper timing of DNA replication relative to the bacterial cell cycle. Control of ATP binding to regulate the replication activity of DnaA protein is apparently important in the proper timing of DNA replication in E. coli.
Full text of research interests