TY - JOUR
T1 - The salvage/turnover/repair (STOR) model for uniparental inheritance in Chlamydomonas
T2 - DNA as a source of sustenance
AU - Sears, B. B.
AU - Vanwinkle-swift, K.
N1 - Funding Information:
From the Department of Botany and Plant Pathology, Michigan State University, Ea»t Lansing, Ml 48824-1312 (Sears) and the Department of Biological Sciences, Northern Arizona University, Flagstaff, AZ 86011 (VanWinkle-Swift). This article is based on presentations given at the American Genetic Association Symposium on Non-Mendelian Inheritance at Michigan State University, March 26-28,1993. We thank Nick Gillham and John Boynton for introducing us to the fascination of Chlamydomonas chioroplast genetics. Thanks also to L Mets, M. Tunnel, B. Smith-White, and H. Bertrand for helpful comments. NSF grants DMB-9019488 and DMB-9106008 are acknowledged for support
PY - 1994
Y1 - 1994
N2 - The non-Mendetian inheritance of chloroplast genes in Chlamydomonas has engaged researchers for decades and has prompted numerous debates regarding molecular mechanisms and evolutionary significance. The hallmarks of chioroplast inheritance in Chlamydomonas are reviewed here, including observations on vegetative haploid cells, somatic hybrids, meiotic zygospores, and vegetative zygotes resulting from sexual reproduction. Models invoked to explain the typical uniparental maternal inheritance of chloroplast genes, and which center upon the presumed existence of sex-specific protectors and destroyers of chloroplast genomes, are briefly discussed. In an effort to bring together the diverse observations on chloroplast gene inheritance in somatic as well as sexual cells, a model is proposed that focuses on organelle DNA turnover as a source of sustenance for the cell during periods of starvation. The salvage/turnover/repair (STOR) model for chloroplast inheritance in Chlamydomonas proposes that as a consequence of the high ploidy of the chloroplast genome, many copies are dispensable; their degradation would provide nucleotides for recombination, repair, RNA synthesis and cell metabolism. The STOR model offers an alternative view of uniparental inheritance as a phenomenon of direct selective benefit to the organism rather than simply being of selfish benefit to the chloroplast genome. These concepts may also have application to other lower eukaryotes that have sexual reproduction coupled with an extended dormancy.
AB - The non-Mendetian inheritance of chloroplast genes in Chlamydomonas has engaged researchers for decades and has prompted numerous debates regarding molecular mechanisms and evolutionary significance. The hallmarks of chioroplast inheritance in Chlamydomonas are reviewed here, including observations on vegetative haploid cells, somatic hybrids, meiotic zygospores, and vegetative zygotes resulting from sexual reproduction. Models invoked to explain the typical uniparental maternal inheritance of chloroplast genes, and which center upon the presumed existence of sex-specific protectors and destroyers of chloroplast genomes, are briefly discussed. In an effort to bring together the diverse observations on chloroplast gene inheritance in somatic as well as sexual cells, a model is proposed that focuses on organelle DNA turnover as a source of sustenance for the cell during periods of starvation. The salvage/turnover/repair (STOR) model for chloroplast inheritance in Chlamydomonas proposes that as a consequence of the high ploidy of the chloroplast genome, many copies are dispensable; their degradation would provide nucleotides for recombination, repair, RNA synthesis and cell metabolism. The STOR model offers an alternative view of uniparental inheritance as a phenomenon of direct selective benefit to the organism rather than simply being of selfish benefit to the chloroplast genome. These concepts may also have application to other lower eukaryotes that have sexual reproduction coupled with an extended dormancy.
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U2 - 10.1093/oxfordjournals.jhered.a111481
DO - 10.1093/oxfordjournals.jhered.a111481
M3 - Article
C2 - 7963452
AN - SCOPUS:0027994286
SN - 0022-1503
VL - 85
SP - 366
EP - 376
JO - Journal of Heredity
JF - Journal of Heredity
IS - 5
ER -