Abstract
An investigation of the mechanism of the polAexl mutation in vitro suggested that the excision repair deficiency observed in vivo does not result from an inability of the enzyme to nick translate. The defect appears to reside in the inability of the enzyme to effectively generate a nick structure to serve as a substrate for DNA ligase.
Publication Date
1-1-1983
Journal Title
Journal of Bacteriology
Document Type
Article
Recommended Citation
Alan F. Wahl, Joel W. Hockensmith, Stanley P. Kowalski & Robert A. Bambara, "Alternative explanation for excision repair deficiency caused by the polAex1 mutation,” 155 J. Bacteriol 922 (1983), available at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC217772/