James E. Haber

Biosketch

James E. Haber was born in Pittsburgh, PA in 1943. He received his AB from Harvard College and his PhD in Biochemistry at the University of California, Berkeley in 1970. After postdoctoral work at the University of Wisconsin, Madison, he joined the Department of Biology at Brandeis University in 1972. He is now the Abraham and Etta Goodman Professor of Biology and Director of the Rosenstiel Basic Medical Sciences Research Center. He has focused his research on genome instability, especially the repair of chromosome double-strand DNA breaks and the role of DNA damage checkpoints. In 2011 he received the Genetics Society of America’s Thomas Hunt Morgan Medal for Lifetime Achievement in Genetics. He is a member of the National Academy of Sciences, and a Fellow of the American Association for the Advancement of Science, the American Academy of Microbiology and the American Academy of Arts and Sciences. He serves as a representative of the Genetics Society of America to the Coalition of Life Sciences.

Research Interests

Haber's lab focuses on mechanisms of DNA repair, especially of double-strand chromosome breaks, primarily using budding yeast as a model organism. His lab has developed assays for the study of nonhomologous end-joining and microhomology-mediated end-joining as well as for several pathways of homologous recombination, including gene conversion, break-induced replication and single-strand annealing. A major interest is in the the way homologous sequences are searched for within the nucleus and the tolerance of the repair machinery for mismatched recombining partners in mitotic and meiotic cells. Another focus is the high rate of mutations arising during otherwise accurate DNA repair. These studies have extended to understanding the mechanism of gene editing by CRISPR/Cas9-mediated single-strand template repair. Recently his lab has become interested in the homologous recombination mechanisms by which the Lyme disease bacterium can "change its coat" to avoid immune surveillance. In addition, his lab continues to study the DNA damage response wherein even a single double-strand break can trigger cell cycle arrest.