Disease relevance of sbcB

• The sbcB coding sequence contains many non-optimal codons, characteristic of many poorly expressed E. coli genes [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].
• At the right terminus, the relevant junction sequences from MRV and myxoma could not be cloned in wild-type Escherichia coli but were maintained stably in a recA recBC sbcB host [3].

High impact information on sbcB

• We propose that DNA replication drives the extrusion of palindromic sequences in vivo, forming secondary structures that are substrates for the recBC and sbcB gene products [4].
• Determination of the nucleotide sequence for the exonuclease I structural gene (sbcB) of Escherichia coli K12 [1].
• The results strongly suggest that 3' (rho) 5' single-stranded DNA ends constitute an important component in recombination pathway involved in DNA double-strand break repair and that absence of sbcB from deinococcal genome may significantly aid its extreme radioresistance phenotype [5].
• The gene is located at min 44 of the E. coli genetic map, close to the sbcB gene. sbmC expression is induced by DNA-damaging agents and, also, by the entry of cells into the stationary growth phase [6].
• A strain containing a deletion of the sbcB gene showed little dRpase activity; the activity could be restored by transformation of the strain with a plasmid containing the sbcB gene [7].

Chemical compound and disease context of sbcB

• Chromosomal transductants (recombinants) were distinguished from plasmid transductants by their ampicillin-sensitive phenotype, or plasmid transductants were avoided by using a recBC sbcB E. coli strain as recipient [8].

Biological context of sbcB

• The rate of recombination of circular dimer plasmids was at least 1000-fold higher in recB recC sbcB or recB recC sbcA mutants as compared to wild-type cells [9].
• Physical analysis of linear dimer- or circular dimer-transformed recB recC sbcB mutants revealed that all transformants contained recombinant monomer genotypes [9].
• In addition, mutation in either sbcA or sbcB supresses the Vrm- phenotype of dam-3 recB21 recC22 strains [10].
• When relocated to the recQ site on the chromosome, the recQ::Tn3 mutations conferred partial resistance to thymineless death (TLD) or, in the case of a recBC sbcB background, recombination deficiency and increased UV sensitivity [11].
• They also act with sbcB mutations as cosuppressors of the defects in recombination, DNA repair, and cell viability associated with recBC mutations [12].

Regulatory relationships of sbcB

• The mechanism by which an sbcB mutation suppresses the deficiency in postreplication repair shown by recB recC mutants of Escherichia coli was studied [13].

Other interactions of sbcB

• Indirect but not direct stimulation was also dependent on recJ (coding for a 5'-to-3' exonuclease specific for single-stranded DNA) regardless of sbcA or sbcB configuration [14].
• The results also show that the recF144 mutation in recBC sbcB recF and recF cells leads to the absence of detectable amounts of a 49,000 molecular weight protein [15].
• This requirement is suppressed by either an additional sbcA or sbcC mutation, but not by an sbcB mutation [16].
• Cultures of recBC sbcB (sbcC+) strains grow slowly, contain many inviable cells, and rapidly accumulate fast-growing variants due to mutation of sbcC. sbcC has been identified on recombinant plasmids and tentatively located by Tn1000 mutagenesis to a 0.9-kilobase DNA section between proC and phoR [17].
• 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].

References