RecQ DNA helicase is a suppressor of illegitimate recombination in Escherichia coli

Abstract

Bloom syndrome and Werner syndrome are genetic disorders in which an increased rate of chromosomal abnormality is observed. The genes responsible for these diseases, BLM and WRN, have been cloned and identified as homologs of the Escherichia coli recQ genes. We studied the effect of recQ mutations on illegitimate recombination, which is an aberrant biological event related to the chromosomal abnormality in humans, and found that a variety of recQ mutations increased spontaneous illegitimate recombination by 20-to 300-fold and increased UV light-induced illegitimate recombination by 10-to 100-fold. Most bio or pro transducing phages are formed by the recombination events at several hot spots, which are enhanced by the recQ mutation. The analysis of nucleotide sequences at the recombination junction in the transducing phages indicates that recombination at the hot spot sites as well as the non-hot spot sites takes place between short homologous sequences. Enhancement of the recombination in the recQ mutants also occurs in the recA, recBC sbcBC, or recBC sbcA backgrounds, indicating that these recombination events are mediated by none of the known recombination pathways, RecBC, RecF, and RecE. We therefore concluded that the RecQ function suppresses illegitimate recombination that depends on short homologous regions. We discuss a model, based on the 3-to-5 helicase activity of RecQ, to explain the role of this protein as a suppressor of illegitimate recombination.

Bloom's syndrome gene suppresses premature ageing caused by Sgs1 deficiency in yeast

“…In E. coli, RecQ helicase is involved in homologous and illegitimate recombination (Nakayama et al 1984;Hanada et al 1997). In yeast, Sgs1 protein physically interacts with topoisomerase II and III (Watt et al 1995(Watt et al , 1996.…”

Escherichia coli HU protein suppresses DNA‐gyrase‐mediated illegitimate recombination and SOS induction

“…Illegitimate recombination can be classified into two classes, shorthomology-dependent illegitimate recombination (SHDIR) and short-homology-independent illegitimate recombination (SHIIR) (Shimizu et al 1997). There have been many reports of illegitimate recombination taking place preferentially between short regions of homology on plasmid or chromosomal DNA (Albertini et al 1982;Jones et al 1982;Marvo et al 1983;Yi et al 1988;Kumagai & Ikeda 1991;Yamaguchi et al 1995;Hanada et al 1997;Shanado et al 1997). These regions usually contain 4-10 base pairs of homologous DNA.…”

Deficient DNA repair in the human progeroid disorder, Werner syndrome

“…Mutations in E. coli RecQ and in the S. cerevisiae RecQ homolog, Sgs1, result in an increased frequency of illegitimate recombination [1]. In humans, defects in three RecQ family members, WRN, Blooms syndrome (BLM), and RECQL4, are associated with rare autosomal-recessive disorders characterized by genomic instability and increased cancer susceptibility.…”