[en] The ³²P damage in R factor DNA and its repair were assayed in minicells by calculation of a fraction of covalently closed circular (CCC) DNA in alkaline sucrose gradient sedimentation. It was shown that conversion of CCC DNA into slower sedimenting components, as well as inactivation of R factor transfer ability, are caused by unrepaired single-strand breaks. There are two mechanisms of repair of single strand breaks produced by ³²P disintegration. The rapid repair, which may be identical or related to rapid repair of X-ray damage mediated by pol 1 gene, is as efficient in dar₄^- and dar₅^- mutants as in wild type. It is so rapid that about 50 percent of single-strand breaks Are repaired before sedimentation analysis is performed. The slow repair, that may be related to slow repair of X-ray damage controlled by rec A gene, is completed after more than one hour incubation. The slow repair of damaged R factor DNA in minicells is less efficient than in the bacterial cell: it is absent in dar₄^- mutant. It is suggested that the slow repair activity is connected with bacterial chromosome, in minicells (i.e. in the polar regions of cells) its amount is limited and is enough to repair ca 5 lesions per molecule. In dar₄^- mutant this activity is lacking in extrachromosomal regions of the cell. (author)