Kent G. Golic
Professor
Department of Biology
Huntsman Cancer Institute
United States of America
Biography
Kent Golic, PhD, is a professor in the department of Biology at the University of Utah. He is an investigator at the Huntsman Cancer Institute and a member of the Nuclear Control of Cell Growth and Differentiation program.Dr. Golic’s research goal is to understand the cellular responses to telomere loss using Drosophila melanogaster (common fruit fly) as a model. In the male germline, cells that carry a chromosome that has lost a telomere frequently survive, and the non-telomeric end is healed by the addition of a new telomere. Telomeres are protein/nucleic acid structures at the ends of linear chromosomes that prevent the cell from interpreting the end as a DNA double-strand break. In general, when a somatic cell detects that a chromosome is missing a telomere, that cell will undergo apoptosis. This induced cell suicide is useful to prevent the proliferation of cells with damaged genomes, such as cancer cells. However, some cells do escape apoptosis and continue to divide, and this is accompanied by accumulation of genomic damage, a hallmark of most cancer cells. Golic’s lab is identifying and characterizing the genes that regulate these cell growth control pathways.Golic received a PhD from the University of Washington and completed postdoctoral training at the University of Chicago.
Research Interest
Genetics Cell Biology Chromosome Structure and Function Telomeres Drosophila Genetic Technologies
Publications
-
Brodsky MH, Weinert BT, Tsang G, Rong YS, McGinnis NM, Golic KG, Rio DC, Rubin GM (2004). Drosophila melanogaster MNK/Chk2 and p53 regulate multiple DNA repair and apoptotic pathways following DNA damage. Mol Cell Biol, 24(3), 1219-31.
-
Titen SW, Golic KG (2008). Telomere loss provokes multiple pathways to apoptosis and produces genomic instability in Drosophila melanogaster. Genetics, 180(4), 1821-32.
-
Titen SW, Golic KG (2010). Healing of euchromatic chromosome breaks by efficient de novo telomere addition in Drosophila melanogaster. Genetics, 184(1), 309-12.
-
Kurzhals RL, Titen SW, Xie HB, Golic KG (2011). Chk2 and p53 are haploinsufficient with dependent and independent functions to eliminate cells after telomere loss. PLoS Genet, 7(6), e1002103.
-
Xie HB, Cammarato A, Rajasekaran NS, Zhang H, Suggs JA, Lin HC, Bernstein SI, Benjamin IJ, Golic KG (2013). The NADPH metabolic network regulates human alphaB-crystallin cardiomyopathy and reductive stress in Drosophila melanogaster. PLoS Genet, 9(6), e1003544.
