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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
1998-12-17
pubmed:abstractText
The recA locus of pathogenic mycobacteria differs from that of non-pathogenic species in that it contains large intervening sequences termed protein introns or inteins that are excised by an unusual protein-splicing reaction. In addition, a high degree of illegitimate recombination has been observed in the pathogenic Mycobacterium tuberculosis complex. Homologous recombination is the main mechanism of integration of exogenous nucleic acids in M. smegmatis, a non-pathogenic mycobacterium species that carries an inteinless RecA and is amenable to genetic manipulations. To investigate the function of recA in mycobacteria, recA- strains of M. smegmatis were generated by allelic exchange techniques. These strains are characterized (i) by increased sensitivity towards DNA-damaging agents [ethylmethylsulphonate (EMS), mitomycin C, UV irradiation] and (ii) by the inability to integrate nucleic acids by homologous recombination. Transformation efficiencies using integrative or replicative vectors were not affected in recA- mutants, indicating that in mycobacteria RecA does not affect plasmid uptake or replication. Complementation of the recA- mutants with the recA from M. tuberculosis restored resistance towards EMS, mitomycin C and UV irradiation. Transformation of the complemented strains with suicide vectors targeting the pyrF gene resulted in numerous allelic exchange mutants. From these data, we conclude that the intein apparently does not interfere with RecA function, i.e. with respect to competency for homologous recombination, the RecAs from pathogenic and non-pathogenic mycobacteria are indistinguishable.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0950-382X
pubmed:author
pubmed:issnType
Print
pubmed:volume
29
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1203-14
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:9767588-Alleles, pubmed-meshheading:9767588-Bacterial Proteins, pubmed-meshheading:9767588-Blotting, Southern, pubmed-meshheading:9767588-Cell Division, pubmed-meshheading:9767588-Cloning, Molecular, pubmed-meshheading:9767588-Ethyl Methanesulfonate, pubmed-meshheading:9767588-Gene Deletion, pubmed-meshheading:9767588-Genetic Vectors, pubmed-meshheading:9767588-Mitomycin, pubmed-meshheading:9767588-Mutagenesis, Insertional, pubmed-meshheading:9767588-Mutagens, pubmed-meshheading:9767588-Mycobacterium smegmatis, pubmed-meshheading:9767588-Mycobacterium tuberculosis, pubmed-meshheading:9767588-Phenotype, pubmed-meshheading:9767588-Protein Splicing, pubmed-meshheading:9767588-Rec A Recombinases, pubmed-meshheading:9767588-Recombination, Genetic, pubmed-meshheading:9767588-Transformation, Bacterial, pubmed-meshheading:9767588-Ultraviolet Rays
pubmed:year
1998
pubmed:articleTitle
Investigation of mycobacterial recA function: protein introns in the RecA of pathogenic mycobacteria do not affect competency for homologous recombination.
pubmed:affiliation
Institut für Medizinische Mikrobiologie, Medizinische Hochschule Hannover, Germany.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't