Publication: Defects associated with mitochondrial DNA damage can be mitigated by increased vacuolar pH in Saccharomyces cerevisiae
dc.contributor.department | Department of Molecular Biology and Genetics | |
dc.contributor.department | Graduate School of Sciences and Engineering | |
dc.contributor.kuauthor | Dunn, Cory David | |
dc.contributor.kuauthor | Garipler, Görkem | |
dc.contributor.schoolcollegeinstitute | College of Sciences | |
dc.contributor.schoolcollegeinstitute | GRADUATE SCHOOL OF SCIENCES AND ENGINEERING | |
dc.date.accessioned | 2024-11-09T23:53:20Z | |
dc.date.issued | 2013 | |
dc.description.abstract | While searching for mutations that alleviate detrimental effects of mitochondrial DNA (mtDNA) damage, we found that disrupting vacuolar biogenesis permitted survival of a sensitized yeast background after mitochondrial genome loss. Furthermore, elevating vacuolar pH increases proliferation after mtDNA deletion and reverses the protein import defect of mitochondria lacking DNA. | |
dc.description.indexedby | WOS | |
dc.description.indexedby | Scopus | |
dc.description.indexedby | PubMed | |
dc.description.issue | 1 | |
dc.description.openaccess | YES | |
dc.description.publisherscope | International | |
dc.description.sponsoredbyTubitakEu | N/A | |
dc.description.sponsorship | National Institutes of Health [T32GM07445] We thank Hiromi Sesaki, Gulayse Ince Dunn, Nurhan Ozlu, Halil Kavakli, and Nebibe Mutlu for review of this manuscript. Special thanks to Rob Jensen at Johns Hopkins School of Medicine, in whose laboratory suppressors of the petite-negative phenotype were isolated using funds from a National Institutes of Health predoctoral training grant (T32GM07445) to C.D.D. Further support for this work was provided by Koc University's College of Sciences and by a European Molecular Biology Organization Installation grant to C.D.D. | |
dc.description.volume | 194 | |
dc.identifier.doi | 10.1534/genetics.113.149708 | |
dc.identifier.issn | 0016-6731 | |
dc.identifier.quartile | Q2 | |
dc.identifier.scopus | 2-s2.0-84877098900 | |
dc.identifier.uri | https://doi.org/10.1534/genetics.113.149708 | |
dc.identifier.uri | https://hdl.handle.net/20.500.14288/14997 | |
dc.identifier.wos | 318274900028 | |
dc.keywords | Slow-growth phenotype | |
dc.keywords | Aaa protease complex | |
dc.keywords | Yeast-cells | |
dc.keywords | Functional mitochondria | |
dc.keywords | Petite mutation | |
dc.keywords | Life-span | |
dc.keywords | Atpase | |
dc.keywords | Membrane | |
dc.keywords | Proteins | |
dc.keywords | Subunit | |
dc.language.iso | eng | |
dc.publisher | Genetics Soc Am | |
dc.relation.ispartof | Genetics | |
dc.subject | Genetics | |
dc.subject | Heredity | |
dc.title | Defects associated with mitochondrial DNA damage can be mitigated by increased vacuolar pH in Saccharomyces cerevisiae | |
dc.type | Journal Article | |
dspace.entity.type | Publication | |
local.contributor.kuauthor | Garipler, Görkem | |
local.contributor.kuauthor | Dunn, Cory David | |
local.publication.orgunit1 | GRADUATE SCHOOL OF SCIENCES AND ENGINEERING | |
local.publication.orgunit1 | College of Sciences | |
local.publication.orgunit2 | Department of Molecular Biology and Genetics | |
local.publication.orgunit2 | Graduate School of Sciences and Engineering | |
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