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Dennis M. Livingston

Emeritus Faculty

Expertise:

 

Research Description

Dr. Livingston’s recent work has focused on the final steps of DNA replication. When DNA is replicated on the lagging strand template, the ends of Okazaki fragments must be tailored by removal of the primer sequence. The nascent fragments are then joined. The removal of primers is the responsibility of the flap endonuclease and the joining is the responsibility of DNA ligase I. We have shown using a genetic analysis that the two enzymes are likely to act in concert.


Recent Publications

Karanja, K.K. and Livingston, D.M. (2009) C-terminal flap endonuclease (rad27) mutations: lethal interactions with a DNA ligase I mutation (cdc9-p) and suppression by proliferating cell nuclear antigen (POL30) in Saccharomyces cerevisiae. Genetics 183:63-78.

Kim, H. and Livingston, D.M.  (2009) Suppression of a DNA polymerase delta mutation by the absence of the high mobility group protein Hmo1 in Saccharomyces cerevisiae.  Curr. Genet. 55:127-138.

Kim, H. and Livingston, D.M.  (2006) A high mobility group protein binds to long CAG repeat tracts and establishes their chromatin organization in Saccharomyces cerevisiae.  J. Biol. Chem.  281:15735-15740.

Refsland, E.W. and Livingston, D.M.  (2005)  Interactions among DNA ligase I, the flap endonuclease and proliferating cell nuclear antigen in the expansion and contraction of CAG repeat tracts in yeast.  Genetics 171:923-934.

Schweitzer, J.K., Reinke, S.S. and Livingston, D.M. (2001) Meiotic alterations in CAG repeat tracts. Genetics  159:1861-1865.

Ireland, M.J., Reinke, S.S. and Livingston, D.M. (2000)  The impact of lagging strand replication mutations on the stability of CAG repeat tracts in yeast. Genetics  155:1657-1665.

P:
Telephone: (612) 625-9479
E:

livin001@umn.edu