Dana Carroll

University of Utah


Election Year: 2017
Primary Section: 21, Biochemistry
Secondary Section: 26, Genetics
Membership Type: Member

Biosketch

Dana Carroll is a molecular biologist/biochemist who works largely in the area of DNA repair and recombination. He is best known for his development of genome editing by programmable DNA cleavage, beginning with zinc-finger nucleases. Carroll was born in California and grew up largely in Bethesda, Maryland. He obtained with a BA degree from Swarthmore College, and a PhD from University of California, Berkeley, both in Chemistry. He pursued postdoctoral research with John Paul at the Beatson Institute for Cancer Research in Glasgow, Scotland, and with Donald Brown at the Carnegie Institution Department of Embryology in Baltimore. He joined the University of Utah faculty in 1975 and served as Chair of the Department of Biochemistry from 1985-2009. He received the Novitski Prize from the Genetics Society of America and the Sober Lectureship Award from the American Society for Biochemistry and Molecular Biology. He is a member of the National Academy of Sciences, a member of the American Academy of Arts and Sciences, and a fellow of the American Association for the Advancement of Science.

Research Interests

The key to high-efficiency genome editing is the creation of a highly specific DNA double-strand break in the desired genomic target. The platforms that facilitate this are the programmable nucleases: zinc-finger nucleases, TALENs and CRISPR-Cas. Investigators around the world are applying these reagents to genome manipulations for many purposes in a wide range of species, from research in model organisms, to improvement of crop plants and livestock, to medical applications in humans. Dana Carroll’s laboratory investigates the design of these nucleases, their delivery to cells and organisms, the fundamental DNA repair mechanisms that process the nuclease-induced breaks, and translation of this knowledge to methods for manipulating genomic DNA sequences. There are multiple pathways of double-strand break repair, and manipulating them can enhance desired genome alterations, including new mutations, gene corrections and sequence insertions. Past work in the Carroll lab showed that disabling the dominant mutagenic pathway increases the recovery of precise corrections and insertions. Current work focuses on the role of chromatin structure in determining the efficiency of nuclease cleavage at various genomic targets.

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