Control of cell division in yeast using the ionophore, A23187 with calcium and magnesium

Duffus, John H.; Patterson, Linda

doi:10.1038/251626a0

Cited by 48 publications

(24 citation statements)

References 7 publications

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“…Pressman demonstrated the cation discrimination patterns of certain ionophorous antibiotics by measuring complexability with cations in a two-phase distribution system (25,27). With respect to their ability to block ion translocation, these antibiotics exhibit various effects on membrane systems of mitochondria (6,8,11), sarcoplasmic reticulum (2,17), lymphocytes (19,20), platelets (7,21), chloroplasts (33), and microbes (4,11). Thus these ionophorous antibiotics have served as valuable tools for studying dynamic properties of ion-carrier mechanisms in biological membranes.…”

mentioning

confidence: 99%

Salinomycin Effects on Mitochondrial Ion Translocation and Respiration

Mitani

Yamanishi

Miyazaki

et al. 1976

Antimicrob Agents Chemother

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The effects of salinomycin on alkali cation transport and membrane functions in rat liver mitochondria have been investigated. After potassium uptake, stimulated by valinomycin or monazomycin in the presence of adenosine 5'-triphosphate, salinomycin caused rapid release of K+ from mitochondria. Salinomycin reversed valinomycin-or monazomycin-induced oscillatory swelling of mitochondria preloaded with K+, Rb+, and Na+ but was without effect on Li+ or Cs+ preloaded mitochondria. Salinomycin blocked the retention of K+ more effectively than the retention of Rb+ or Na+. Salinomycin inhibited both coupled and uncoupled respiration with strict substrate specificity in medium of low but not in high K+ concentration. The oxidation of glutamate, a-ketoglutarate, and malate plus pyruvate was inhibited by salinomycin, but that of 3-hydroxybutyrate or succinate was not significantly affected. Salinomycin inhibited adenosine triphosphatase activity of mitochondria induced by valinomycin or monazomycin in K+ and Rb+ medium without significantly affecting adenosine triphosphatase activity in Li+, Na+, or Cs+ medium. Oxidative phosphorylation in mitochondria was inhibited by sklinomycin but the inhibitory effect of salinomycin lacked the substrate specificity observed for respiration. It is proposed that salinomycin perturbs mitochondrial functions by acting as a mobile carrier for alkali cations through membranes.

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mentioning

confidence: 99%

Salinomycin Effects on Mitochondrial Ion Translocation and Respiration

Mitani

Yamanishi

Miyazaki

et al. 1976

Antimicrob Agents Chemother

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“…This agent inhibits growth of a variety of yeasts by its action on the integrity of the mitochondrial membrane (3) or, alternatively, by inhibiting the breakdown of microtubules (6). Interestingly, Mg2+ reverses this ionophore's growth inhibition (6), and Mg2+ has been shown to be essential for maintenance of the mitochondrial membrane (3).…”

Section: Resultsmentioning

confidence: 99%

“…a trols. Thus, Nal has a diverse effect on these r2S two yeasts: in the one case it causes a very large increase in the MDT without effecting cell synchrony, and in the other case it effects syn-2_6 6 chrony with only a small increase in the MDT. The toxicity of Nal on DNA, RNA, and pro-were synchronized and counted as described in Matetein metabolism and growth of C. albicans in rials and Methods.…”

Section: Resultsmentioning

confidence: 99%

Toxicity of Nalidixic Acid on Candida albicans, Saccharomyces cerevisiae , and Kluyveromyces lactis

Sobieski

Brewer

1976

Antimicrob Agents Chemother

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The antibacterial drug nalidixic acid (Nal) can suppress the growth of Candida albicans at levels of the drug normally found in urine. Growth suppression increases as drug levels are increased, and Nal also causes a similar proportional inhibition of the synthesis of all cellular macromolecules. However, growth temperature (25 versus 37 C) and the divalent cations Mg 2+ and Mn 2+ can increase C. albicans resistance to Nal. Also, nitrogen depletion of Candida shows that Nal-treated and untreated cells exhibit no difference in leucine uptake during readaptation to nitrogen. In Nal-treated, nitrogen-starved cells, ribonucleic acid and deoxyribonucleic acid (DNA) biosynthesis are less affected than in unstarved Nal-treated cells, but of the two nucleic acids DNA synthesis is the most affected. Nal-resistant strains of C. albicans exhibit a slight toxicity for macromolecular synthesis. Nal treatment of a synchronized population of Saccharomyces cerevisiae results in an increase in the culture mean doubling time of, at most, 20%, but Nal causes the loss of synchronous cell division. With a synchronized population of Kluyveromyces lactis , Nal causes an increase in the mean doubling time of upwards of 300%, with synchrony of cell division being maintained. It is known that S. cerevisiae asynchronously synthesizes mitochondrial DNA during the cell cycle, whereas with K. lactis it is synchronous. Thus, with C. albicans Nal toxicity is dependent both on the dose and the physiological state of the cell. Furthermore, Nal inhibits growth of yeast with synchronous mitochondrial DNA synthesis more adversely than yeast with asynchronous mitochondrial DNA synthesis.

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“…This is particularly true of excitation-contraction 1200 800 400 a '' I I coupling (Frank, 1962;Ebashi, 1974), excitationsecretion coupling (Douglas & Poisner, 1964;Matthews, 1970) and cell division (Duffus & Patterson, 1974). Elegant studies with ciliated protozoa have also established a role of calcium in determining the orientation and frequency of the ciliary beat (Naitoh & Kaneko, 1972).…”

Section: Discussionmentioning

confidence: 99%

Effects of Divalent and Lanthanide Ions on Motility Initiation in Rat Caudal Epididymal Spermatozoa

Lee

Tsang

Wong

1981

British J Pharmacology

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Sperm motility initiation of rat caudal epididymal spermatozoa in vitro has been studied. Spermatozoa flushed out from the cauda epididymis with a sodium‐free medium exhibited a transient motility which decreased progessively. At 40 min, the forward motility was completely suppressed. However, if they were resuspended in a sodium containing medium their motility was completely restored to normal within 15 min. This initiation of sperm motility required the presence of extracellular calcium. Maximal stimulation was obtained at a calcium concentration of 10 −3M. Above this concentration, further increase in calcium produced a fall in motility and at 10 −2M, motility initiation was completely suppressed. The initiation of sperm motility has been shown to depend closely on sodium. Sperm motility initiation alters in a curvilinear fashion with extracellular sodium concentration showing saturation kinetics. High calcium (above 10−3m) was found to depress motility initiation induced by sodium, without affecting the apparent affinity constant for sodium. The effect of Ca2+ on sperm motility initiation could be mimicked by Sr2+ but not by Mg2+, La3+ or Eu3+. In the presence of extracellular calcium (1.27 or 2.54 mM), La3+ and Eu3+ exerted a dose‐dependent inhibition of sperm motility initiation. The IC50 values for both ions were about 5 × l0−5M. The possible mechanism of inhibition by lanthanide ions is discussed.

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Control of cell division in yeast using the ionophore, A23187 with calcium and magnesium

Cited by 48 publications

References 7 publications

Salinomycin Effects on Mitochondrial Ion Translocation and Respiration

Salinomycin Effects on Mitochondrial Ion Translocation and Respiration

Toxicity of Nalidixic Acid on Candida albicans, Saccharomyces cerevisiae , and Kluyveromyces lactis

Effects of Divalent and Lanthanide Ions on Motility Initiation in Rat Caudal Epididymal Spermatozoa

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