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J Bacteriol. 1973 July; 115(1): 153-161
Copyright © 1973 American Society for Microbiology. All Rights Reserved.

Relationship Between Prophage Induction and Transformation in Haemophilus influenzae

Jane K. Setlow, M. E. Boling, D. P. Allison and K. L. Beattie

Biology Division, Oak Ridge National Laboratory, Oak Ridge, Tennessee 37830

ABSTRACT

The interaction between transformation and prophages of HP1c1, S2, and a defective phage of Haemophilus influenzae has been investigated by measurement of (i) the effect of prophage on transformation frequency and (ii) the effect of transformation on phage induction. The presence of any of the prophages does not appreciably alter transformation frequencies in various Rec+ and Rec strains. However, exposure of competent lysogens to transforming deoxyribonucleic acid (DNA) may induce phage but only in Rec+ strains, which are able to integrate transforming DNA into their genome. Transformation of Rec+ lysogens with DNA irradiated with ultraviolet (UV) light causes the production of even more phage than results from unirradiated DNA, but this indirect UV induction is not as effective as direct induction by UV irradiation of lysogens. Both types of UV induction are influenced by the repair capacity of the host. Wild-type cells contain a prophage and can be induced by transformation to produce a defective phage, which kills a small fraction of the cells. Defective phage in wild-type cells are also induced by H. parainfluenzae DNA, and a much larger fraction of the cells is killed. Strain BC200, which is highly transformable but is not inducible for defective phage, is not killed by H. parainfluenzae DNA, suggesting that wild-type cells are killed by killed by this DNA because of phage induction. A minicell-producing mutant, LB11, has been isolated. Some phage induction occurs in this strain when the cells are made competent, unlike the wild type. A large majority of LB11 cells surviving the competence regime are killed by exposure to transforming DNA.


J Bacteriol. 1973 July; 115(1): 153-161
Copyright © 1973 American Society for Microbiology. All Rights Reserved.




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