Disease relevance of recN

• Different effects of recJ and recN mutations on the postreplication repair of UV-damaged DNA in Escherichia coli K-12 [1].
• Recombinant lambda phages that complement the recombination and repair defects of recN recBC sbcB mutants have been identified, and the recN gene has been cloned from these phages into a low copy-number plasmid [2].
• Characterization of the spoIVB and recN loci of Bacillus subtilis [3].
• To investigate the roles of the gonococcal recN and recJ genes in the recombination-based processes of the gonococcus, these genes were inactivated in the N. gonorrhoeae strain FA1090 [4].
• Identification and disruption analysis of the recN gene in the extremely radioresistant bacterium Deinococcus radiodurans [5].

High impact information on recN

• However, the recN-mediated mutagenesis response was found to require the recA gene and the umuDC genes, and could be suppressed in the presence of a plasmid harbouring the SOS transcriptional repressor LexA [6].
• Escherichia coli cells defective for the recN gene display constitutive elevation of mutagenesis at 3,N(4)-ethenocytosine via an SOS-induced mechanism [6].
• Nucleotide sequence and LexA regulation of the Escherichia coli recN gene [7].
• Mutation of recN reduced sectored recombinants in these crosses to approximately 1% in all the strains examined, including recD [8].
• We report that both recN and recJ loss-of-function mutants show decreased DNA repair ability [4].

Biological context of recN

• Overlapping functions of recD, recJ and recN provide evidence of three epistatic groups of genes in Escherichia coli recombination and DNA repair [9].
• The basis for this phenotype was investigated by monitoring the properties associated with recN mutations in otherwise wild-type strains [2].
• The minimal inducing dose in uvrA and recN mutants was lower than in the wild-type, whereas their SOS response was higher at all doses [10].
• These results imply that recN cells are constitutively active for SOS mutagenesis functions [6].
• Two independent genes, recN and spoIVB, along with their respective promoter and termination regions, were discovered and sequenced in the 3.4-kilobase region between the ahrC and spoOA genes at map position 216 in the Bacillus subtilis chromosome map [3].

Other interactions of recN

• However, no synergistic interactions were discovered between recG258 and mutations in recF, recN, or recQ [11].
• In the recBCsbcBC strain and isogenic recL and recN derivatives basal recA expressions were 3- to 5-fold higher than that of wild-type cells and were inducible by mitomycin C [12].
• (iii) Mutations in two more SOS-inducible genes, recN and recQ, do not decrease the repair [13].
• Mutation of the recN gene of Escherichia coli in a recBC sbcB genetic background blocks conjugational recombination and confers increased sensitivity to UV light and mitomycin C [2].
• In contrast, frequencies of RecET-mediated illegitimate recombination were not affected by ruvAB, ruvC, recG, and recN mutations [14].

Analytical, diagnostic and therapeutic context of recN

• This mutant, as well as a previously characterized recN mutant (recN262), showed a markedly decreased frequency of excision of Tn10 after treatment with UV or mitomycin C [15].
• Northern blot experiments confirmed radiation activation of the recA and recN genes at a dose of 2 Gy [16].

References