Abstract
Two new genetic loci of Bacillus subtilis are identified by mutations that confer resistance to distamycin A and to other antibacterial agents. The chromosomal region where they map probably contains a cluster of genes whose products are related to membrane structure and function. Some of the biological effects of distamycin A are still in evidence in the resistant mutants indicating that the drug possibly acts at multiple sites. Most biological effects of the drug (including the phenotypic correction of a morphopoietic mutation) are likely to be due to the interaction of distamycin A with membrane (or surface) structures.
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