By Robert K. Poole
First released in 1967, Advances in Microbial body structure is one among Elsevier's most famed and acclaimed sequence. Now edited by means of Professor Robert Poole, college of Sheffield, Advances in Microbial body structure keeps to post topical and demanding experiences, analyzing body structure in its broadest context, to incorporate all fabric that contributes to our figuring out of ways microorganisms and their part components paintings. issues contain: * Glutathione, Altruistic Metabolite in Fungi * The function of the Flavodiiron Proteins in Microbial Nitric Oxide cleansing * tension Responsive micro organism: Biosensors as Environmental screens * Bacterial Na+ -or H+ - coupled ATP working at low electrochemical power * Dissimiatory Fe(III) and Mn(IV) relief
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Extra resources for Advances in Microbial Physiology, Vol. 49
2003b). A possible pathway for the degradation of exogenous GSH could involve a membrane-bound carboxypeptidase releasing glycine and a cyclotransferase-type enzyme releasing cysteine in the cytosol. , 1996) but not in fungi. Saccharomyces cerevisiae cells respond to sulfur deprivation by increasing the turnover rate of GSH and channelling the sulfur content of GSH into cysteine and methionine to maintain protein synthesis at an acceptable level. , 1991). The mobilization of intracellular GSH reserves under sulfur starvation was also demonstrated in P.
2003). 6. 1. Nitrogen Starvation In S. cerevisiae cells exposed to nitrogen deprivation, about 90% of total GSH accumulated in the central vacuole and a transitory stimulation of GSH biosynthesis was also observed (Mehdi and Penninckx, 1997). The transient overproduction of GSH was inhibited by buthionine-(S,R)sulfoximine, a speciﬁc transition-state-analogue inhibitor of gGCS and was absent in a GSH-deﬁcient strain (Mehdi and Penninckx, 1997). The transport of GSH molecules into the vacuoles was mainly (about 70%) Ycf1p-dependent and a vATPase-coupled system also contributed to this process (about 30%).
G. , 1988). The former product is transported into the vacuoles by Ycf1p and is metabolized further to dimethylamine, CS2 and H2S, which are all released into the culture medium (Elskens and Penninckx, 1997). Alternatively, the GS-X GSS(S ¼ )CN(CH3)2 can react with GSH, which further increase the intracellular DMDT concentration with the concomitant depletion of the GSH pool (Elskens and Penninckx, 1995a, 1997). The re-oxidation of 44 ISTVA´N PO´CSI, ROLF A. PRADE AND MICHEL J. PENNINCKX DMTD to Thiram by cytochrome c initiates a deleterious redox re-cycling process, which, together with the inactivation of GR by both Thiram and DMTD, prevents the re-establishment of a physiologically relevant GSH/GSSG balance (Elskens and Penninckx, 1995b).
Advances in Microbial Physiology, Vol. 49 by Robert K. Poole