Cellular Responses to Mitochondrial DNA Damage in Yeast

Ruth Stuckey (Editor)
M.Carmen Díaz de la Loz (Editor)
Ralf Erik Wellinger (Editor)
Universidad de Sevilla – CSIC, Sevilla, Spain

Series: Cell Biology Research Progress, DNA and RNA: Properties and Modifications, Functions and Interactions, Recombination and Applications
BISAC: SCI056000

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Volume 10

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Volume 2

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Special issue: Resilience in breaking the cycle of children’s environmental health disparities
Edited by I Leslie Rubin, Robert J Geller, Abby Mutic, Benjamin A Gitterman, Nathan Mutic, Wayne Garfinkel, Claire D Coles, Kurt Martinuzzi, and Joav Merrick

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The nuclear and mitochondrial genomes are both subject to various types of DNA damage caused by exogenous sources, such as ultraviolet (UV) radiation, genotoxic drugs, and to endogenous damage like continuously produced reactive oxygen species (ROS). Persistent DNA damage will be encountered by the replication and transcription machineries and has been shown to result in a decay of DNA and RNA synthesis. Failed repair and replication can lead to mutation or loss of both nuclear and mitochondrial DNA (mtDNA).

In addition to the aging process, many human diseases have been associated with mtDNA mutation or copy number dysregulation, including muscular dystrophies and cancer. Therefore, there is an increased need to understand how cells maintain a functional mitochondrial genome. This book discusses known mtDNA repair pathways and explore the cellular consequences of mitochondrial dysfunction observed in yeast, including petite formation, changes in mitochondrial morphology and copy number. (Imprint: Nova)

ABSTRACT

INTRODUCTION

MITOCHONDRIA ARE A SOURCE OF DNA DAMAGE

REPAIR OF MTDNA

REGULATION OF REPAIR ENZYME TARGETING

MITOCHONDRIAL DNA COPY NUMBER REGULATION

MITOCHONDRIAL MORPHOLOGY

NUCLEAR INSTABILITY CAUSED BY MITOCHONDRIAL DYSFUNCTION

CONCLUSION

REFERENCES

INDEX

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