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Pathways and Mechanisms that Prevent Genome Instability in Saccharomyces cerevisiae

Genome rearrangements result in mutations that underlie many human diseases, and ongoing genome instability likely contributes to the development of many cancers. The tools for studying genome instability in mammalian cells are limited, whereas model organisms such as Saccharomyces cerevisiae are mo...

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Autores principales: Putnam, Christopher D., Kolodner, Richard D.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Genetics Society of America 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5500125/
https://www.ncbi.nlm.nih.gov/pubmed/28684602
http://dx.doi.org/10.1534/genetics.112.145805
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author Putnam, Christopher D.
Kolodner, Richard D.
author_facet Putnam, Christopher D.
Kolodner, Richard D.
author_sort Putnam, Christopher D.
collection PubMed
description Genome rearrangements result in mutations that underlie many human diseases, and ongoing genome instability likely contributes to the development of many cancers. The tools for studying genome instability in mammalian cells are limited, whereas model organisms such as Saccharomyces cerevisiae are more amenable to these studies. Here, we discuss the many genetic assays developed to measure the rate of occurrence of Gross Chromosomal Rearrangements (called GCRs) in S. cerevisiae. These genetic assays have been used to identify many types of GCRs, including translocations, interstitial deletions, and broken chromosomes healed by de novo telomere addition, and have identified genes that act in the suppression and formation of GCRs. Insights from these studies have contributed to the understanding of pathways and mechanisms that suppress genome instability and how these pathways cooperate with each other. Integrated models for the formation and suppression of GCRs are discussed.
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spelling pubmed-55001252017-07-07 Pathways and Mechanisms that Prevent Genome Instability in Saccharomyces cerevisiae Putnam, Christopher D. Kolodner, Richard D. Genetics YeastBook Genome rearrangements result in mutations that underlie many human diseases, and ongoing genome instability likely contributes to the development of many cancers. The tools for studying genome instability in mammalian cells are limited, whereas model organisms such as Saccharomyces cerevisiae are more amenable to these studies. Here, we discuss the many genetic assays developed to measure the rate of occurrence of Gross Chromosomal Rearrangements (called GCRs) in S. cerevisiae. These genetic assays have been used to identify many types of GCRs, including translocations, interstitial deletions, and broken chromosomes healed by de novo telomere addition, and have identified genes that act in the suppression and formation of GCRs. Insights from these studies have contributed to the understanding of pathways and mechanisms that suppress genome instability and how these pathways cooperate with each other. Integrated models for the formation and suppression of GCRs are discussed. Genetics Society of America 2017-07 2017-06-29 /pmc/articles/PMC5500125/ /pubmed/28684602 http://dx.doi.org/10.1534/genetics.112.145805 Text en Copyright © 2017 by the Genetics Society of America Available freely online through the author-supported open access option.
spellingShingle YeastBook
Putnam, Christopher D.
Kolodner, Richard D.
Pathways and Mechanisms that Prevent Genome Instability in Saccharomyces cerevisiae
title Pathways and Mechanisms that Prevent Genome Instability in Saccharomyces cerevisiae
title_full Pathways and Mechanisms that Prevent Genome Instability in Saccharomyces cerevisiae
title_fullStr Pathways and Mechanisms that Prevent Genome Instability in Saccharomyces cerevisiae
title_full_unstemmed Pathways and Mechanisms that Prevent Genome Instability in Saccharomyces cerevisiae
title_short Pathways and Mechanisms that Prevent Genome Instability in Saccharomyces cerevisiae
title_sort pathways and mechanisms that prevent genome instability in saccharomyces cerevisiae
topic YeastBook
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5500125/
https://www.ncbi.nlm.nih.gov/pubmed/28684602
http://dx.doi.org/10.1534/genetics.112.145805
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