Études sur le chondriome de la levure

Yotsuyanagi, Y

doi:10.1016/s0022-5320(62)80032-x

Cited by 101 publications

(18 citation statements)

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“…The lack of oxidative activities in anaerobic yeast is not associated with a complete absence of mitochondrial membrane profiles (Swift, Rabinowitz, and Getz, 1967 ;Swift, Rabinowitz, and Getz, 1968 ;Plattner and Schatz, 1969) . This situation is reminiscent of that observed in the mitochondrial mutants, where recognizable (cytoplasmic mutants) and in some cases normal (chromosomal mutants) mitochondrial structures are seen without any evident terminal respiratory activity (Yotsuyanagi, 1962) . Thus both in anaerobically grown yeast and in certain mutant yeasts, microscopically identifiable mitochondrial membranes and characteristic mitochondrial function do not develop in parallel .…”

Section: Introductionmentioning

confidence: 72%

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Cardiolipin Content of Wild Type and Mutant Yeasts in Relation to Mitochondrial Function and Development

Jakovcic

Getz

Rabinowitz

et al. 1971

The Journal of Cell Biology

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The phospholipid composition of various strains of the yeast, Saccharomyces cerevisiae, and several of their derived mitochondrial mutants grown under conditions designed to induce variations in the complement of mitochondrial membranes has been examined . Wild type and petite (cytoplasmic respiratory deficient) yeasts were fractionated into various subcellular fractions, which were monitored by electron microscopy and analyzed for cytochrome oxidase (in wild type) and phospholipid composition . 90% or more of the phospholipid, cardiolipin was found in the mitochondrial membranes of wild type and petite yeast . Cardiolipin content differed markedly under various growth conditions . Stationary yeast grown in glucose had better developed mitochondria and more cardiolipin than repressed log phase yeast . Aerobic yeast contained more cardiolipin than anaerobic yeast . Respiration-deficient cytoplasmic mitochondrial mutants, both suppressive and neutral, contained less cardiolipin than corresponding wild types . A chromosomal mutant lacking respiratory function had normal cardiolipin content . Log phase cells grown in galactose and lactate, which do not readily repress the development of mitochondrial membranes, contained as much cardiolipin as stationary phase cells grown in glucose . Cytoplasmic mitochondrial mutants respond to changes in the glucose concentration of the growth medium by variations in their cardiolipin content in the same way as wild type yeast does under similar growth conditions. It is concluded that cardiolipin content of yeast is correlated with, and is a good indicator of, the state of development of mitochondrial membrane .

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Section: Introductionmentioning

confidence: 72%

“…(c) Cytoplasmic mutants, both suppressive and neutral petite, have relatively poorly developed mitochondrial profiles (Yotsuyanagi, 1962) and virtually no respiratory capacity . These mutants also contain less cardiolipin than the corresponding wild type cells (Tables V and VI) .…”

Section: Cells Grown In Chemostatmentioning

confidence: 99%

Cardiolipin Content of Wild Type and Mutant Yeasts in Relation to Mitochondrial Function and Development

Jakovcic

Getz

Rabinowitz

et al. 1971

The Journal of Cell Biology

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“…These enzymes include cytochromes a and b and certain dehydrogenases (see Slonimski, 1953). The cytoplasmic mutant known as 'petite' lacks these enzymes (Sherman & Slonimski, 1964;Roodyn & Wilkie, 1967a) and has no inner mitochondrial membrane (Yotsuyanagi, 1962). The mutational change to petite is apparently irreversible and the notation p -is generally applied to this class of mutant inferring loss of genetic information.…”

Section: Introductionmentioning

confidence: 99%

Inhibition of mitochondrial synthesis in yeast by erythromycin: cytoplasmic and nuclear factors controlling resistance

1968

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Erythromycin-resistant mutants were separated into two categories showing Mendelian and non-Mendelian inheritance of resistance respectively. The cytoplasmic factor was located in the mitochondrion based on the fact that the loss of the mitochondrial genetic unit associated with the petite mutation (the ρ factor, assumed to be the mitochondrial DNA) resulted in a corresponding permanent loss of resistance. Conversely, the petite mutation in gene resistant mutants had no effect on the inheritance of resistance.Analysis of vegetative and sexual progeny of isolated zygotes from a number of crosses between resistant and sensitive strains indicated that different mitochondrial types, both sensitive and resistant, co-exist in the yeast cell and are distributed at random among daughter cells under non-selective conditions. Only resistant mitochondria are in evidence if zygotes are put down to proliferate on medium containing the antibiotic.Resistant strains were tested for retention of resistance following anaerobic culture (known to cause disruption of mitochondria). The cytoplasmic mutants retained their resistance but two gene-resistant mutants tested both lost their resistance. It was suggested in the latter case that resistance is dependent on the existence of intact mitochondrial membrane (possibly inner membrane). In the former mutants the mechanism of resistance may be the alteration of one or other of the components of the protein-synthesizing system of the organelle.

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“…Accordingly, the ratios of C18 to C16 in the sufficient and the deficient yeast (9). However, in the yeast cells grown under anaerobic conditions, this membrane structure was not observed, but when the cells contacted oxygen these mitochondrial membranes were formed accompanied by the respiratory activity (10,11). Okuda and Takahashi showed that PaA deficient cells had no detectable res piratory activities and that cytochrome oxidase activity in the mitochondria was markedly reduced.…”

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confidence: 99%