Abstract
With roles in DNA repair, recombination, replication and transcription, members of the RecQ DNA helicase family maintain genome integrity from bacteria to mammals. Mutations in human RecQ helicases BLM, WRN and RecQL4 cause incurable disorders characterized by genome instability, increased cancer predisposition and premature adult-onset aging. Yeast cells lacking the RecQ helicase Sgs1 share many of the cellular defects of human cells lacking BLM, including hypersensitivity to DNA damaging agents and replication stress, shortened lifespan, genome instability and mitotic hyper-recombination, making them invaluable model systems for elucidating eukaryotic RecQ helicase function. Yeast and human RecQ helicases have common DNA substrates and domain structures and share similar physical interaction partners. Here, we review the major cellular functions of the yeast RecQ helicases Sgs1 of Saccharomyces cerevisiae and Rqh1 of Schizosaccharomyces pombe and provide an outlook on some of the outstanding questions in the field.
Highlights
We review the major cellular functions of the yeast RecQ helicases Sgs1 of Saccharomyces cerevisiae and Rqh1 of Schizosaccharomyces pombe and provide an outlook on some of the outstanding questions in the field
Disruption of RecQ significantly reduces recombination frequency and increases sensitivity to ultraviolet (UV) radiation of cells in which recombination events are prevented from proceeding through RecBCD and SbcBC pathways, identifying RecQ as a member of the alternate RecF recombination pathway [1,6]
Additional protein interactions for the acidic regions contribute to the role of Sgs1 in promoting homologous recombination by acting as a DNA mimic that competes with ssDNA for RPA binding, thereby facilitating the initial loading of
Summary
RecQ-like DNA helicases act as key factors in homologous recombination (HR) and recombinational DNA repair and, in some organisms, perform accessory roles in DNA replication and transcription. Disruption of RecQ significantly reduces recombination frequency and increases sensitivity to ultraviolet (UV) radiation of cells in which recombination events are prevented from proceeding through RecBCD and SbcBC pathways, identifying RecQ as a member of the alternate RecF recombination pathway [1,6]. In wildtype cells, this RecF pathway appears to mediate genetic exchange at single-strand (ss) DNA gaps and contributes to the repair of collapsed replication forks.
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