Document Detail


Conflicting levels of selection in the accumulation of mitochondrial defects in Saccharomyces cerevisiae.
MedLine Citation:
PMID:  11891344     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The somatic accumulation of defective mitochondria causes human degenerative syndromes, senescence in fungi, and male sterility in plants. These diverse phenomena may result from conflicts between natural selection at different levels of organization. Such conflicts are fundamental to the evolution of cooperating groups, from cells to populations. We present a model in which defective mitochondrial genomes accumulate because of a within-cell replication advantage when among-cell selection for efficient respiration is relaxed. We tested the model by using experimental populations of the yeast Saccharomyces cerevisiae. We constructed yeast strains that were heteroplasmic for mitochondrial mutations that destroy the ability to respire (the petite phenotype) and followed the accumulation of mitochondrial defects in cultures with different effective population sizes. As predicted by the model, the inability to respire evolved only in small populations of S. cerevisiae, where among-cell selection favoring cells that can respire was reduced relative to within-cell selection favoring parasitic mitochondria. In a control experiment, mitochondrial point mutations that confer resistance to chloramphenicol showed no tendency to change in frequency under any culture conditions. The accumulation of some mitochondrial defects is therefore an evolutionary process, involving multiple levels of selection. The relative intensities of within- and among-cell selection may also explain the tissue specificity of human mitochondrial defects.
Authors:
Douglas R Taylor; Clifford Zeyl; Erin Cooke
Related Documents :
25360674 - Rapid screening of different types of antitumor compound groups from traditional chines...
10393984 - The alternative oxidase lowers mitochondrial reactive oxygen production in plant cells.
2876544 - Quantitative evaluation of leukemic mitochondria with a computer-controlled image analy...
22700654 - Reactive oxygen species are involved in the morphology-determining mechanism of fremyel...
16469734 - Regulation of epithelial na+ channels (enac) by methylation: a novel methyltransferase ...
23295384 - Trypanosoma cruzi: effects of heat shock on ecto-atpase activity.
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.     Date:  2002-03-12
Journal Detail:
Title:  Proceedings of the National Academy of Sciences of the United States of America     Volume:  99     ISSN:  0027-8424     ISO Abbreviation:  Proc. Natl. Acad. Sci. U.S.A.     Publication Date:  2002 Mar 
Date Detail:
Created Date:  2002-03-20     Completed Date:  2002-04-24     Revised Date:  2010-09-14    
Medline Journal Info:
Nlm Unique ID:  7505876     Medline TA:  Proc Natl Acad Sci U S A     Country:  United States    
Other Details:
Languages:  eng     Pagination:  3690-4     Citation Subset:  IM    
Affiliation:
Department of Biology, University of Virginia, Charlottesville, VA 22904-4328, USA. drt3b@virginia.edu
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Cell Respiration / drug effects
Chloramphenicol / pharmacology
DNA, Mitochondrial / genetics*
Drug Resistance, Fungal
Evolution, Molecular
Genome
Mitochondria / drug effects,  genetics*,  metabolism,  pathology*
Models, Biological
Mutation / genetics
Saccharomyces cerevisiae / cytology*,  drug effects,  genetics*
Selection, Genetic*
Chemical
Reg. No./Substance:
0/DNA, Mitochondrial; 56-75-7/Chloramphenicol
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Reelin function in neural stem cell biology.
Next Document:  An unexpected role for brain-type sodium channels in coupling of cell surface depolarization to cont...