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.

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Pharmacological evidence suggests that anion channel-mediated plasma membrane anion effluxes are crucial in early defense signaling to induce immune responses and hypersensitive cell death in plants. However, their molecular bases and regulation remain largely unknown. We overexpressed Arabidopsis SLAC1, an S-type anion channel involved in stomatal closure, in cultured tobacco BY-2 cells and analyzed the effect on cryptogein-induced defense responses including fluxes of Cl− and other ions, production of reactive oxygen species (ROS), gene expression and hypersensitive responses. The SLAC1-GFP fusion protein was localized at the plasma membrane in BY-2 cells. Overexpression of SLAC1 enhanced cryptogein-induced Cl− efflux and extracellular alkalinization as well as rapid/transient and slow/prolonged phases of NADPH oxidase-mediated ROS production, which was suppressed by an anion channel inhibitor, DIDS. The overexpressor also showed enhanced sensitivity to cryptogein to induce downstream immune responses, including the induction of defense marker genes and the hypersensitive cell death. These results suggest that SLAC1 expressed in BY-2 cells mediates cryptogein-induced plasma membrane Cl− efflux to positively modulate the elicitor-triggered activation of other ion fluxes, ROS as well as a wide range of defense signaling pathways. These findings shed light on the possible involvement of the SLAC/SLAH family anion channels in cryptogein signaling to trigger the plasma membrane ion channel cascade in the plant defense signal transduction network.