RECQ DNA HELICASE IS A SUPPRESSOR OF ILLEGITIMATE RECOMBINATION IN ESCHERICHIA-COLI

Bloom syndrome and Werner syndrome are genetic disorders in which an i ncreased rate of chromosomal abnormality is observed. The genes respon sible 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, an d found that a variety of recQ mutations increased spontaneous illegit imate recombination by 20- to 300-fold and increased UV light-induced illegitimate recombination by 10- to 100-fold. Most lambda bio or lamb da pro transducing phages are formed by the recombination events at se veral hot spots, which are enhanced by the recQ mutation. The analysis of nucleotide sequences at the recombination junction in the transduc ing phages indicates that recombination at the hot spot sites as well as the non-hot spot sites takes place between short homologous sequenc es. Enhancement of the recombination in the recQ mutants also occurs i n the recA, recBC sbcBC, or recBC sbcA backgrounds, indicating that th ese recombination events are mediated by none of the known recombinati on pathways, RecBC, RecF, and RecE. We therefore concluded that the Re cQ function suppresses illegitimate recombination that depends on shor t homologous regions. We discuss a model, based on the 3'-to-5' helica se activity of RecQ, to explain the role of this protein as a suppress or of illegitimate recombination.