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Chapter category: Aging

Yeast RecQ Helicases: Clues to DNA Repair, Genome Stability and Aging

This chapter appears in the following book:

Molecular Mechanisms of Werner's Syndrome

Edited by: Michel Lebel
ISBN: 0-306-48233-9
» Get more information about this book at landesbioscience.com «

Chapter authors:
Rozalyn M. Anderson and David A. Sinclair


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The budding yeast Saccharomyces cerevisiae has been used as model for a wide range of cellular processes, including those related to the RecQ-associated progeroid disease, Werner’s syndrome (WS). Investigations of RecQ function in these lower eukaryotes have produced a large body of data that is directly relevant to the function of the Werner’s syndrome helicase, WRN, and other human RecQ members such as BLM. The yeasts studies point to a role for eukaryotic RecQ helicases in a number of key activities associated with DNA repair and replication, including the resolution of aberrant DNA structures, recombinational DNA repair, suppression of illegitimate recombination and the intra-S phase DNA damage checkpoint. Biochemical studies demonstrate that the budding yeast RecQ helicase, Sgs1, resolves the same DNA substrates as the human RecQ enzymes, suggesting that they share a common function. Many of the proteins that interact with Sgs1 also interact with WRN or BLM, further highlighting the relevance of the yeast studies. Mutation of SGS1 results in telomere defects and symptoms of premature aging, two features of WS. Like WS cells, sgs1 mutants also have phenotypes that are not aging-related and most likely stem from defects in recombinational repair and DNA damage signaling.

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Additional chapters from this book:

Replicative Senescence, Telomeres and Werner’s Syndrome

Richard G.A. Faragher

Werner’s syndrome (WS) is studied as a model of accelerated aging and results from mutations in a recQ helicase (WRN). WS fibroblasts show a mutator phenotype (producing large DNA deletions), replic...

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Clinical Aspects of Werner’s Syndrome: Its Natural History and the Genetics of the Disease

Makoto Goto

Werner’s syndrome, caused by a mutation in the WRN (or RecQ3) helicase gene, shows a variety of clinical and biochemical-aging phenotypes at an early stage of life followed by death at an average ag...

Yeast RecQ Helicases: Clues to DNA Repair, Genome Stability and Aging

Rozalyn M. Anderson and David A. Sinclair

The budding yeast Saccharomyces cerevisiae has been used as model for a wide range of cellular processes, including those related to the RecQ-associated progeroid disease, Werner’s syndrome (WS). In...

Biochemical Characterization of the Werner Syndrome DNA Helicase—Exonuclease

Michael Fry

The positional cloning in 1996 of WRN, the human gene defective in Werner syndrome (WS), launched an explosive experimental activity that culminated in the expression, purification and comprehensive c...

Biochemical Roles of RecQ Helicases

Payam Mohaghegh and Ian D. Hickson

The RecQ family of DNA helicases appears to influence DNA repair, replication and/or homologous recombination pathways. In humans, a defect in the RecQ family helicases encoded by the BLM, WRN a...

Sensitivity of Werner's Syndrome Cells to DNA Damaging Agents: Insights into the Biological Functions of the Werner Protein

Adayabalam S. Balajee and Fabrizio Palitti

Werner’s syndrome (WS) is a human autosomal recessive disorder characterized by many symptoms of accelerated aging. The gene responsible for Werner’s syndrome (WRN) has been cloned and the protein has...

Potential Function of the Werner's Syndrome Homologue in the African Clawed Frog and the Mouse

Michel Lebel and Philip Leder

After the discovery of the gene responsible for WS in the human, genes with high homology to WRN were found in the mouse Mus musculus and the African clawed frog Xenopus laevis genome. These lab...


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