Transmission of mitochondrial and chloroplast genomes in crosses of Chlamydomonas.

Boynton, John E.; Harris, Elizabeth H.; Burkhart, Bryce D.; Lamerson, Patrick M.; Gillham, Nicholas W.

doi:10.1073/pnas.84.8.2391

Cited by 138 publications

(69 citation statements)

References 30 publications

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“…On the other hand, the evidence of mtDNA complementation and recombination clearly indicates that mitochondrial fusion does occur in other organisms, such as S. cerevisiae (10), Chlamydomonas spp. (6), and plants (39,46). However, it has also been found in yeast cells that, in p+ x p+ crosses, mtDNA mixing is not extensive and appears to be limited to that portion of the zygote which gives rise to medial buds and, furthermore, that the sorting of mtDNA is controlled differently from that of the bulk matrix protein constituents (3).…”

Section: Discussionmentioning

confidence: 99%

Complementation of mutant and wild-type human mitochondrial DNAs coexisting since the mutation event and lack of complementation of DNAs introduced separately into a cell within distinct organelles.

1994

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The rules that govern complementation of mutant and wild-type mitochondrial genomes in human cells were investigated under different experimental conditions. Among mitochondrial transformants derived from an individual affected by the MERRF (myoclonus epilepsy associated with ragged red fibers) encephalomyopathy and carrying in heteroplasmic form the mitochondrial tRNALYS mutation associated with that syndrome, normal protein synthesis and respiration was observed when the wild-type mitochondrial DNA exceeded 10% of the total complement. In these transformants, the protective effect of wild-type mitochondrial DNA was shown to involve interactions of the mutant and wild-type gene products. Very different results were obtained in experiments in which two mitochondrial DNAs carrying nonallelic disease-causing mutations were sequentially introduced within distinct organelles into the same human mitochondrial DNA-less (p°) cell. In transformants exhibiting different ratios of the two genomes, no evidence of cooperation between their products was observed, even 3 months after the introduction of the second mutation. These results pointed to the phenotypic independence of the two genomes. A similar conclusion was reached in experiments in which mitochondria carrying a chloramphenicol resistance-inducing mitochondrial DNA mutation were introduced into chloramphenicol-sensitive cells. A plausible interpretation of the different results obtained in the latter two sets of experiments, compared with the complementation behavior observed in the heteroplasmic MERRF transformants, is that in the latter, the mutant and wild-type genomes coexisted in the same organelles from the time of the mutation. This would imply that the way in which mitochondrial DNA is sorted among different organelles plays a fundamental role in determining the oxidative-phosphorylation phenotype in mammalian cells. These results have significant implications for mitochondrial genetics and for studies on the transmission and therapy of mitochondrial DNA-linked diseases.Despite the large number of studies on the expression of artificially produced mitochondrial DNA (mtDNA) mutations and the phenotype of somatic cell hybrids and cybrids, information on mitochondrial genome interactions in mammalian cells is still very limited. The dependence of such interactions on the distribution of the mtDNA molecules among the mitochondria, which changes continuously throughout division and, possibly, fusion of the organelles, and the difficulty of investigating mtDNA sorting in a cell account in part for the present lack of understanding of how much the mitochondrial genomes interact in mammalian cells. The recent discovery of a variety of mtDNA mutations associated with diseases in humans (47) and the growing evidence of accumulation of mtDNA mutations with aging in somatic tissues (12-14, 19, 43) have raised a number of questions about the occurrence and frequency of intermixing of mutant and wild-type mtDNA and/or their products within a cell and the role that co...

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Section: Discussionmentioning

confidence: 99%

Complementation of mutant and wild-type human mitochondrial DNAs coexisting since the mutation event and lack of complementation of DNAs introduced separately into a cell within distinct organelles.

1994

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“…The null growth phenotype of these mutants under heterotrophic conditions was inherited by the mating type minus parent, a characteristic of a genetic lesion located in the mitochondrial genome [42].…”

Section: Genetics Of Chlamydomonas To Isolate Respiratory-deficient Mmentioning

confidence: 99%

Respiratory-deficient mutants of the unicellular green alga Chlamydomonas: A review

et al. 2014

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Genetic manipulation of the unicellular green alga Chlamydomonas reinhardtii is straightforward. Nuclear genes can be interrupted by insertional mutagenesis or targeted by RNA interference whereas random or site-directed mutagenesis allows the introduction of mutations in the mitochondrial genome. This, combined with a screen that easily allows discriminating respiratorydeficient mutants, makes Chlamydomonas a model system of choice to study mitochondria biology in photosynthetic organisms. Since the first description of Chlamydomonas respiratory-deficient mutants in 1977 by random mutagenesis, many other mutants affected in mitochondrial components have been characterized. These respiratory-deficient mutants increased our knowledge on function and assembly of the respiratory enzyme complexes. More recently some of these mutants allowed the study of mitochondrial gene expression processes poorly understood in Chlamydomonas. In this review, we update the data concerning the respiratory components with a special focus on the assembly factors identified on other organisms. In addition, we make an inventory of different mitochondrial respiratory mutants that are inactivated either on mitochondrial or nuclear genes. Opposed Reviewers:Claire Remacle -Génétique des microorganismes -Institut de Botanique B22 Boulevard du Rectorat, 27 -Université de Liège-B-4000 Liège, Belgique Tel +32 4 3663812 -Fax +32 4 3663840 e-mail: c.remacle@ulg.ac.be First, we wish to thank the two anonymous reviewers for their constructive comments. We found their suggestions very helpful to improve the quality of our manuscript. We have addressed all the points they raised and have modified the text accordingly. A detailed response to reviewers' comments is included below.We believe we have addressed all referees' comments and we hope this revised version is now suitable for publication in Biochimie.We are looking forward to hearing from you, With best regards, Cover LetterResponse to reviewers The text has been modified in order to give more background details on the methodology used to create and screen respiratory mutants in Chlamydomonas. The main modifications correspond to: Paragraph 2.3: -p8. A figure (Fig. 4) has been added in order to provide more information on dark-dier/slow growth screens for different classes of mutant.-p9. The mitochondrial transformation method used in Chlamydomonas has been detailed.Paragraph 2.4: -p10. The TTC-based screen has been explained.Finally, all along the text the methods used to create nuclear and mitochondrial mutants has been indicated. Also, the text could benefit from being proof-read by a native English speaker as the grammar is a little awkward in places. I highlight a couple of points below, but there are a number of other places where the English could be improved for clarity.The text has been proof-read by a good English speaker as requested and the text has been modified according to the comments.Minor points:1. Abstract, line 1: "the genetics" have been replaced by "genetic manipu...

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“…Boynton et al (1987) Whether the mt+ or mt-parent carried the mutation, the diploids showed a paternal inheritance frequency of between 100 and 56%, depending on the experiment. Thus, the vegetative diploids showed biparental mtDNA inheritance.…”

Section: No Methylation Of Mtdnamentioning

confidence: 99%

“…Experiments showing the paternal inheritance of mtDNA in Chlamydomonas Boynton et al (1987) crossed interspecific strains of C. smithii mt+ with C. reinhardtii mt-and analyzed the resulting progeny based on physical differences in restriction fragment patterns between the organelle genomes of these strains. A reciprocal cross was also conducted.…”

Section: Chlamydomonasmentioning

confidence: 99%

Mitochondria inherit its DNA from male parents in Chlamydomonas

Nakamura

Aoyama

2011

PL. MORPH.

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Transmission of mitochondrial and chloroplast genomes in crosses of Chlamydomonas.

Cited by 138 publications

References 30 publications

Complementation of mutant and wild-type human mitochondrial DNAs coexisting since the mutation event and lack of complementation of DNAs introduced separately into a cell within distinct organelles.

Complementation of mutant and wild-type human mitochondrial DNAs coexisting since the mutation event and lack of complementation of DNAs introduced separately into a cell within distinct organelles.

Respiratory-deficient mutants of the unicellular green alga Chlamydomonas: A review

Mitochondria inherit its DNA from male parents in Chlamydomonas

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