title: Two closely related RecQ helicases have antagonistic roles in homologous recombination and DNA repair in Arabidopsis thaliana.
abstract: RecQ helicases are involved in the processing of DNA structures arising during replication, recombination, and repair throughout all kingdoms of life. Mutations of different RecQ homologues are responsible for severe human diseases, such as Blooms (BLM) or Werner (WRN) syndrome. The loss of RecQ function is often accompanied by hyperrecombination caused by a lack of crossover suppression. In the Arabidopsis genome seven different RecQ genes are present. Two of them (AtRECQ4A and 4B) arose because of a recent duplication and are still nearly 70% identical on a protein level. Knockout of these genes leads to antagonistic phenotypes: the RECQ4A mutant shows sensitivity to DNA-damaging agents, enhanced homologous recombination (HR) and lethality in a mus81 background. Moreover, mutation of RECQ4A partially suppresses the lethal phenotype of an AtTOP3alpha mutant, a phenomenon that had previously been demonstrated for RecQ homologues of unicellular eukaryotes only. Together, these facts strongly suggest that in plants RECQ4A is functionally equivalent to SGS1 of Saccharomyces cerevisiae and the mammalian BLM protein. In stark contrast, mutants of the closely related RECQ4B are not mutagen-sensitive, not viable in a mus81 background, and unable to suppress the induced lethality caused by loss of TOP3alpha. Moreover, they are strongly impaired in HR. Thus, AtRECQ4B is specifically required to promote but not to suppress crossovers, a role in which it differs from all eukaryotic RecQ homologues known.
authors.affiliation: Botany II, University Karlsruhe, Kaiserstrasse 12, D-76128 Karlsruhe, Germany.
authors.forename: Frank
authors.initials: F
authors.lastname: Hartung
authors.forename: Stefanie
authors.initials: S
authors.lastname: Suer
authors.forename: Holger
authors.initials: H
authors.lastname: Puchta
mesh_terms: D017360:Arabidopsis / Q000187:drug effects / Q000235:genetics* / Q000254:growth & development / Q000378:metabolism*; D029681:Arabidopsis Proteins / Q000235:genetics / Q000378:metabolism; D001483:Base Sequence; D001761:Bleomycin / Q000633:toxicity; D002945:Cisplatin / Q000633:toxicity; D004260:DNA Repair / Q000235:genetics*; D004264:DNA Topoisomerases, Type I / Q000235:genetics / Q000378:metabolism; D004269:DNA, Bacterial / Q000235:genetics; D018744:DNA, Plant / Q000235:genetics*; D004720:Endonucleases / Q000235:genetics / Q000378:metabolism; D015971:Gene Expression Regulation, Enzymologic; D018506:Gene Expression Regulation, Plant; D009154:Mutation / Q000235:genetics; D010641:Phenotype; D053484:RecQ Helicases / Q000037:antagonists & inhibitors* / Q000235:genetics / Q000378:metabolism*; D011995:Recombination, Genetic / Q000235:genetics*; D012680:Sensitivity and Specificity
chemical_list: D029681:Arabidopsis Proteins; D004269:DNA, Bacterial; D018744:DNA, Plant; C036483:T-DNA; D001761:Bleomycin; D004720:Endonucleases; C514438:MUS81 protein, Arabidopsis; D053484:RecQ Helicases; D004264:DNA Topoisomerases, Type I; D002945:Cisplatin