Journal of Bacteriology, May 2001, p. 2963-2968, Vol. 183, No. 9
0021-9193/01/$04.00+0 DOI: 10.1128/JB.183.9.2963-2968.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Department of Microbiology and Immunology, Temple University School of Medicine, Philadelphia, Pennsylvania 19140,1 and Institute of Cell & Molecular Biology, University of Edinburgh, Edinburgh EH9 3JR, Scotland2
Received 24 October 2000/Accepted 6 February 2001
The major role of RecA is thought to be in helping repair and restart stalled replication forks. During exponential growth, Bacillus subtilis recA cells exhibited few microscopically observable nucleoid defects. However, the efficiency of plating was about 12% of that of the parent strain. A substantial and additive defect in viability was also seen for addB and recF mutants, suggesting a role for the corresponding recombination paths during normal growth. Upon entry into stationary phase, a subpopulation (~15%) of abnormally long cells and nucleoids developed in B. subtilis recA mutants. In addition, recA mutants showed a delay in, and a diminished capacity for, effecting prespore nucleoid condensation.
Present address: Department of Molecular Biology, Princeton
University, Princeton, NJ 08544.
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