Greehey CCRI Spring Seminar Series: James Haber, PhD (Brandeis Univ)
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Repair of broken chromosomes and triggering of the DNA damage response
View lectures from James Haber
Broken chromosomes must be repaired if a cell is to survive; consequently, cells have evolved a variety of mechanisms to repair double-strand breaks (DSBs). Both homologous recombination, in which the ends of the broken DNA seek out intact templates with the same sequence, and nonhomologous end-joining pathways are found in Saccharomyces as they are in humans. In addition, cells have evolved a damage-sensing checkpoint system that delays entry into mitosis until the break has been repaired.
Analysis of homologous recombination.
Recombination between homologous sequences is a fundamental process in both meiosis and mitotic cells. We are interested in understanding, at the molecular level, how recombination occurs and the roles of the many proteins involved in DNA recombination, repair, and replication. Using synchronized cells undergoing recombination initiated at a specific site on a chromosome by an inducible endonuclease, we use physical monitoring techniques (Southern blots, PCR analysis) to follow the sequence of molecular events in real time. We are interested in determining what are the specific biochemical roles played by the many proteins implicated in DNA recombination, repair and replication. This “in vivo biochemistry” approach has enabled us to demonstrate that there are several independent, competing pathways of homologous recombination, each with its own genetic requirements.
Learn more about Dr. Haber’s research.