Literature DB >> 12202624

A colony color method identifies the vulnerability of mitochondria to oxidative damage.

Grace Kim1, Hashmat Sikder, Keshav K Singh.   

Abstract

Mitochondrial dysfunction is a profound feature of cancer cells and is also known to cause several mitochondrial diseases. Mutations in mitochondrial DNA (mtDNA) have been reported frequently in these diseases. Although many environmental agents are known to cause damage to mitochondria, rapid methods need to be developed for testing agents that cause mitochondrial dysfunction and are involved in the development of mitochondrial and other diseases. Using Saccharomyces cerevisiae, we describe the development of a colorimetric method that identifies both physical and chemical agents that cause mitochondrial dysfunction and mutation of the mitochondrial genome. This method utilizes the previously reported ade2 mutant of S.cerevisiae that produces red colonies. However, when they lose mitochondrial function the colonies turn white. This colorimetric method has helped quantify the vulnerability of mtDNA to oxidative agents. Our study reveals that the oxidative agent adriamycin causes both mutation and extensive damage to mtDNA, which leads to loss of mtDNA. Our study also reveals that the lost mtDNA fragments migrate to the nucleus and integrate into the nuclear genome. Furthermore, our analysis reveals that loss of mtDNA leads to resistance to oxidative agents. The method described in this paper should aid in the rapid identification of environmental and other agents that cause mitochondrial dysfunction and mutagenesis, agents that may be involved in the development of mitochondrial and other diseases.

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Year:  2002        PMID: 12202624     DOI: 10.1093/mutage/17.5.375

Source DB:  PubMed          Journal:  Mutagenesis        ISSN: 0267-8357            Impact factor:   3.000


  11 in total

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2.  mip1 containing mutations associated with mitochondrial disease causes mutagenesis and depletion of mtDNA in Saccharomyces cerevisiae.

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Journal:  Br J Pharmacol       Date:  2012-11       Impact factor: 8.739

4.  Yeast as a model of human mitochondrial tRNA base substitutions: investigation of the molecular basis of respiratory defects.

Authors:  Arianna Montanari; Céline Besagni; Cristina De Luca; Veronica Morea; Romina Oliva; Anna Tramontano; Monique Bolotin-Fukuhara; Laura Frontali; Silvia Francisci
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5.  Flucytosine antagonism of azole activity versus Candida glabrata: role of transcription factor Pdr1 and multidrug transporter Cdr1.

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6.  Generation and analysis of a barcode-tagged insertion mutant library in the fission yeast Schizosaccharomyces pombe.

Authors:  Bo-Ruei Chen; Devin C Hale; Peter J Ciolek; Kurt W Runge
Journal:  BMC Genomics       Date:  2012-05-03       Impact factor: 3.969

7.  Genome-wide distribution of RNA-DNA hybrids identifies RNase H targets in tRNA genes, retrotransposons and mitochondria.

Authors:  Aziz El Hage; Shaun Webb; Alastair Kerr; David Tollervey
Journal:  PLoS Genet       Date:  2014-10-30       Impact factor: 5.917

8.  High-resolution mapping of heteroduplex DNA formed during UV-induced and spontaneous mitotic recombination events in yeast.

Authors:  Yi Yin; Margaret Dominska; Eunice Yim; Thomas D Petes
Journal:  Elife       Date:  2017-07-17       Impact factor: 8.140

9.  Overexpression of mitochondrial oxodicarboxylate carrier (ODC1) preserves oxidative phosphorylation in a yeast model of Barth syndrome.

Authors:  Maxence de Taffin de Tilques; Déborah Tribouillard-Tanvier; Emmanuel Tétaud; Eric Testet; Jean-Paul di Rago; Jean-Paul Lasserre
Journal:  Dis Model Mech       Date:  2017-02-10       Impact factor: 5.758

10.  Genetic interaction network of the Saccharomyces cerevisiae type 1 phosphatase Glc7.

Authors:  Michael R Logan; Thao Nguyen; Nicolas Szapiel; James Knockleby; Hanting Por; Megan Zadworny; Michael Neszt; Paul Harrison; Howard Bussey; Craig A Mandato; Jackie Vogel; Guillaume Lesage
Journal:  BMC Genomics       Date:  2008-07-15       Impact factor: 3.969

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