Different sources of acidity in glucose-elicited extracellular acidification in the yeast Saccharomyces cerevisiae.
Three wild-type strains of Saccharomyces cerevisiae, viz. K, Y55 and sigma 1278b, two mutants lacking one or both of the putative K+ transporters, trk1 delta and trk1 delta trk2 delta, and a mutant in the plasma membrane H(+)-ATPase, viz. pma1-105, were compared in their extracellular acidification following addition of glucose and subsequent addition of KCl; in ATPase activity in purified plasma membranes; and in respiration on glucose. The glucose-induced acidification was the greater the higher the respiratory quotient, i.e. the higher the anaerobic metabolism. A markedly lower acidification was found in the ATPase-deficient pma1-105 strain but also in the TRK-deficient double mutant. The acidification pattern after addition of KCl corresponds to expectations in the TRK mutants; however, a similarly decreased acid production was found in the ATPase-deficient mutant pma1-105. The highest rate of ATP hydrolysis in vitro was found with the trk1 delta trk2 delta mutant where glucose-, as well as KCl-induced acidification were lowest. Likewise, the pma1-105 mutant with extremely low acidification showed only a minutely lower ATP hydrolysis than did its parent Y55 strain. Apparently, several different sources of acidity are involved in the glucose-induced acidification (including extrusion of organic acids); in fact, contrary to the general belief, the H(+)-ATPase may play a minor role in this process in some strains.
Lapathitis
G
G
Institute of Physiology, Prague 4, Czech Republic.
Kotyk
A
A
D000143:Acids / Q000378:metabolism*; D000255:Adenosine Triphosphate / Q000378:metabolism; D001692:Biological Transport; D002412:Cations / Q000378:metabolism; D002462:Cell Membrane / Q000378:metabolism; D004923:Erythrosine / Q000494:pharmacology; D005800:Genes, Fungal / Q000235:genetics; D005947:Glucose / Q000378:metabolism* / Q000494:pharmacology; D017506:H(+)-K(+)-Exchanging ATPase / Q000235:genetics / Q000378:metabolism; D006863:Hydrogen-Ion Concentration; D006868:Hydrolysis / Q000187:drug effects; D007700:Kinetics; D009154:Mutation; D011188:Potassium / Q000378:metabolism; D054328:Proton Pump Inhibitors; D012441:Saccharomyces cerevisiae / Q000187:drug effects / Q000201:enzymology / Q000235:genetics / Q000378:metabolism*; D013468:Suloctidil / Q000494:pharmacology; D014638:Vanadates / Q000494:pharmacology
D000143:Acids; D002412:Cations; D054328:Proton Pump Inhibitors; D014638:Vanadates; D000255:Adenosine Triphosphate; D017506:H(+)-K(+)-Exchanging ATPase; D005947:Glucose; D004923:Erythrosine; D011188:Potassium; D013468:Suloctidil