This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Volff, J. N. Articles by Altenbuchner, J. Search for Related Content PubMed PubMed Citation Articles by Volff, J. N. Articles by Altenbuchner, J.

 Previous Article  |  Next Article 

J. Bacteriol., Apr 1997, 2440-2445, Vol 179, No. 7
Copyright © 1997, American Society for Microbiology

Influence of disruption of the recA gene on genetic instability and genome rearrangement in Streptomyces lividans

JN Volff and J Altenbuchner
Institut fur Industrielle Genetik, Universitat Stuttgart, Germany.

Streptomyces lividans TK23 gives rise to chloramphenicol-sensitive (Cml(s)) mutants at a frequency of about 0.5%. This is due to the frequent occurrence of very large chromosomal deletions removing the corresponding chloramphenicol resistance gene. A mutant in which the recA gene has been disrupted (S. lividans FrecD3 [G. Muth, D. Frese, A. Kleber, and W. Wohlleben, personal communication]) segregated about 70 times more chloramphenicol-sensitive mutants than the parental strain. An enhancement of the deletion frequency was responsible for this mutator phenotype. The amplifiable locus AUD1 has a duplicated structure in some S. lividans strains and is frequently highly amplified in some mutants generated by genetic instability. The chromosomal AUD1 is not amplified in strain TK23 because of the lack of one duplication. Nevertheless, AUD1-derived amplifiable units presenting the typical duplicated organization amplified very well in TK23 when carried on a plasmid. No amplification of these units was observed in the recA mutant. The ability to amplify was restored when the wild-type recA gene was introduced into the plasmid carrying the amplifiable unit. These results suggest that the RecA protein plays a role in reducing the level of genetic instability and chromosomal deletions and show that the recA gene is necessary to achieve high-copy- number amplification of AUD1.

This article has been cited by other articles:

• Wang, L., Yu, Y., He, X., Zhou, X., Deng, Z., Chater, K. F., Tao, M. (2007). Role of an FtsK-Like Protein in Genetic Stability in Streptomyces coelicolor A3(2). J. Bacteriol. 189: 2310-2318 [Abstract] [Full Text]  
• Uchida, T., Miyawaki, M., Kinashi, H. (2003). Chromosomal Arm Replacement in Streptomyces griseus. J. Bacteriol. 185: 1120-1124 [Abstract] [Full Text]  
• Vierling, S., Weber, T., Wohlleben, W., Muth, G. (2001). Evidence that an Additional Mutation Is Required To Tolerate Insertional Inactivation of the Streptomyces lividans recA Gene. J. Bacteriol. 183: 4374-4381 [Abstract] [Full Text]  
• Vierling, S., Weber, T., Wohlleben, W., Muth, G. (2000). Transcriptional and Mutational Analyses of the Streptomyces lividans recX Gene and Its Interference with RecA Activity. J. Bacteriol. 182: 4005-4011 [Abstract] [Full Text]