Sue Jinks-Robertson is a geneticist recognized for her work on mechanisms that contribute to genetic stability and instability of eukaryotic genomes. She is particularly known for her studies of transcription-associated mutagenesis and the regulation of recombination fidelity in yeast. Jinks-Robertson was born and grew up on the Gulf Coast in Panama City, Florida. She attended Agnes Scott College, a liberal arts women’s college in Decatur, Georgia, and graduated in 1977 with a degree in Biology. She obtained a PhD in Genetics from the University of Wisconsin, Madison in 1983 where her research focused on the regulation of ribosome biosynthesis in bacteria. Postdoctoral research was done at The University of Chicago from 1983 to1986 and focused on recombination between dispersed, repeated sequences in yeast. Jinks-Robertson joined the faculty of Emory University in 1987 and moved to Duke University in 2006. She has been active in the Genetics Society of America as a Board member and as Treasurer.

Research Interests

Sue Jinks-Robertson's laboratory uses yeast as a model system to define and understand basic mechanisms that regulate the mitotic stability of eukaryotic genomes. There are two major areas of interest: mutagenesis and recombination. Recombination studies focus on interactions between repeated sequences that are not identical, which can result in genome rearrangements, and how such interactions are prevented by the mismatch repair machinery. In addition, interactions between nonidentical sequences have been used to study the transfer of DNA strands that occurs during recombination between a broken duplex and its intact repair template. Studies of mutagenesis in the Jinks-Robertson lab use reporter constructs to define distinct mutation signatures and then use genetics to link these signatures to specific processes such as replication, mismatch repair, DNA damage bypass and transcription. Recent studies have focused on transcription-related genetic instability, which reflects an increase in damage to the corresponding duplex DNA. Some damage reflects enhanced single-stranded character of the DNA and some reflects mutagenic processing of strand breaks created by topoisomerases that relieve transcription-associated torsional stress.

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Section 26: Genetics