The Absence of the Mitochondrial ATP Synthase  Subunit Promotes a Slow Growth Phenotype of Rho<sup>−</sup> Yeast Cells by a Lack of Assembly of the Catalytic Sector F<sub>1</sub>

Giraud, Marie‐France; Velours, Jean

doi:10.1111/j.1432-1033.1997.00813.x

Cited by 76 publications

(79 citation statements)

References 35 publications

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“…A strain carrying a deletion of ATP3 (subunit ␥) grows very slowly when mtDNA is lacking (321). Strains with deletions of either ATP16 or ATP15, encoding subunits ␦ and ε, respectively, also exhibit slow growth (107). The growth defect of atp3 and atp16 mutants was also noticed by Lai-Zang et al (170).…”

Section: No Compromise: Nuclear Mutants Killed By Mtdna Instability Amentioning

confidence: 71%

Maintenance and Integrity of the Mitochondrial Genome: a Plethora of Nuclear Genes in the Budding Yeast

Contamine

Picard

2000

Microbiol Mol Biol Rev

264

209

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SUMMARY Instability of the mitochondrial genome (mtDNA) is a general problem from yeasts to humans. However, its genetic control is not well documented except in the yeast Saccharomyces cerevisiae. From the discovery, 50 years ago, of the petite mutants by Ephrussi and his coworkers, it has been shown that more than 100 nuclear genes directly or indirectly influence the fate of the rho+ mtDNA. It is not surprising that mutations in genes involved in mtDNA metabolism (replication, repair, and recombination) can cause a complete loss of mtDNA (rho0 petites) and/or lead to truncated forms (rho−) of this genome. However, most loss-of-function mutations which increase yeast mtDNA instability act indirectly: they lie in genes controlling functions as diverse as mitochondrial translation, ATP synthase, iron homeostasis, fatty acid metabolism, mitochondrial morphology, and so on. In a few cases it has been shown that gene overexpression increases the levels of petite mutants. Mutations in other genes are lethal in the absence of a functional mtDNA and thus convert this petite-positive yeast into a petite-negative form: petite cells cannot be recovered in these genetic contexts. Most of the data are explained if one assumes that the maintenance of the rho+ genome depends on a centromere-like structure dispensable for the maintenance of rho− mtDNA and/or the function of mitochondrially encoded ATP synthase subunits, especially ATP6. In fact, the real challenge for the next 50 years will be to assemble the pieces of this puzzle by using yeast and to use complementary models, especially in strict aerobes.

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Section: No Compromise: Nuclear Mutants Killed By Mtdna Instability Amentioning

confidence: 71%

Maintenance and Integrity of the Mitochondrial Genome: a Plethora of Nuclear Genes in the Budding Yeast

Contamine

Picard

2000

Microbiol Mol Biol Rev

264

209

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“…We have previously shown that although mtETC functions are dispensable in transgenic P. falciparum expressing a cytosolic dihydroorotate dehydrogenase, maintenance of mitochondrial membrane potential is essential for other critical functions of the organelle (46). ATP hydrolysis, with or without concomitant proton pumping, by the ATP synthase complex could serve this function as has been shown in other systems (54,59). (ii) Production of ATP is required for the local consumption in the mitochondrion.…”

Section: Discussionmentioning

confidence: 99%

ATP Synthase Complex of Plasmodium falciparum

Nina

Morrisey

Ganesan

et al. 2011

Journal of Biological Chemistry

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Background:The role of ATP synthase in blood stages of malaria parasites has been unclear. Results: Canonical subunits were targeted to the mitochondrion, could not be deleted by gene disruption, and were present in large complexes. Conclusion: Plasmodium ATP synthase is likely essential and forms a dimeric complex. Significance Composition, properties, structure, and drugability of the complex should be fully investigated.

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“…However, the petite mutants have severe growth defects. Like PGS1, ATP15 and ATP16 also were thought to be essential in a petite background (Giraud and Velours, 1997;Lai-Zhang et al, 1999;Contamine and Picard, 2000).…”

Section: Discussionmentioning

confidence: 99%

Loss of Function ofKRE5Suppresses Temperature Sensitivity of Mutants Lacking Mitochondrial Anionic Lipids

Zhong

Gvozdenović-Jeremić

Webster

et al. 2005

MBoC

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Disruption of PGS1, which encodes the enzyme that catalyzes the committed step of cardiolipin (CL) synthesis, results in loss of the mitochondrial anionic phospholipids phosphatidylglycerol (PG) and CL. The pgs1⌬ mutant exhibits severe growth defects at 37°C. To understand the essential functions of mitochondrial anionic lipids at elevated temperatures, we isolated suppressors of pgs1⌬ that grew at 37°C. One of the suppressors has a loss of function mutation in KRE5, which is involved in cell wall biogenesis. The cell wall of pgs1⌬ contained markedly reduced ␤-1,3-glucan, which was restored in the suppressor. Stabilization of the cell wall with osmotic support alleviated the cell wall defects of pgs1⌬ and suppressed the temperature sensitivity of all CL-deficient mutants. Evidence is presented suggesting that the previously reported inability of pgs1⌬ to grow in the presence of ethidium bromide was due to defective cell wall integrity, not from "petite lethality." These findings demonstrated that mitochondrial anionic lipids are required for cellular functions that are essential in cell wall biogenesis, the maintenance of cell integrity, and survival at elevated temperature. INTRODUCTIONCardiolipin (CL), a unique anionic phospholipid with dimeric structure, is ubiquitous in eukaryotes and primarily found in the mitochondrial inner membrane . CL plays a key role in mitochondrial bioenergetics (Jiang et al., 2000; Greenberg, 2000, 2002;Schlame et al., 2000;Pfeiffer et al., 2003) and is also involved in mitochondrial biogenesis (Kawasaki et al., 1999;Jiang et al., 2000). Defective remodeling of CL is associated with Barth syndrome, a severe genetic disorder characterized by cardiomyopathy, neutropenia, skeletal myopathy, and respiratory chain defects (Vreken et al., 2000). The phenotype of Barth syndrome is dependent upon multiple factors that are not well understood (Barth et al., 1983(Barth et al., , 1996. Elucidation of the functions of CL will help to clarify the abnormalities associated with this disorder.The biosynthesis of CL is conserved in eukaryotic organisms. It occurs via three enzymatic reactions , including formation of phosphatidylglycerolphosphate (PGP) from CDP-DAG and glycerol-3-P, dephosphorylation of PGP to phosphatidylglycerol (PG), and condensation of CDP-DAG and PG to form CL. Disruption of PGS1, the structural gene encoding PGP synthase, results in the complete loss of both PG and CL (Janitor et al., 1996;Chang et al., 1998a). The crd1⌬ mutant, which lacks CL synthase, has no detectable CL but accumulates PG (Jiang et al., 1997;Chang et al., 1998b;Tuller et al., 1998;Jiang et al., 2000;Pfeiffer et al., 2003;Zhong et al., 2004). The human taffazin gene (TAZ1), which is associated with Barth syndrome, encodes a transacylase that may be involved in the remodeling of CL (Xu et al., 2003). Deletion of the yeast homolog of this gene, TAZ1, leads to decreased CL, aberrant CL acyl species, and accumulation of monolysocardiolipin . Mutants deficient in CL biosynthesis exhibit growth defects at elevat...

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The Absence of the Mitochondrial ATP Synthase  Subunit Promotes a Slow Growth Phenotype of Rho⁻ Yeast Cells by a Lack of Assembly of the Catalytic Sector F₁

Cited by 76 publications

References 35 publications

Maintenance and Integrity of the Mitochondrial Genome: a Plethora of Nuclear Genes in the Budding Yeast

Maintenance and Integrity of the Mitochondrial Genome: a Plethora of Nuclear Genes in the Budding Yeast

ATP Synthase Complex of Plasmodium falciparum

Loss of Function ofKRE5Suppresses Temperature Sensitivity of Mutants Lacking Mitochondrial Anionic Lipids

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The Absence of the Mitochondrial ATP Synthase  Subunit Promotes a Slow Growth Phenotype of Rho− Yeast Cells by a Lack of Assembly of the Catalytic Sector F1

Cited by 76 publications

References 35 publications

Maintenance and Integrity of the Mitochondrial Genome: a Plethora of Nuclear Genes in the Budding Yeast

Maintenance and Integrity of the Mitochondrial Genome: a Plethora of Nuclear Genes in the Budding Yeast

ATP Synthase Complex of Plasmodium falciparum

Loss of Function ofKRE5Suppresses Temperature Sensitivity of Mutants Lacking Mitochondrial Anionic Lipids

Contact Info

Product

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The Absence of the Mitochondrial ATP Synthase  Subunit Promotes a Slow Growth Phenotype of Rho⁻ Yeast Cells by a Lack of Assembly of the Catalytic Sector F₁