Pentose phosphate pathway mutants of yeast

Abstract

A glucose-negative mutant of Saccharomyces cerevisiae lacking 6-phosphogluconate dehydrogenase, the second enzyme of the pentose phosphate pathway, has been obtained by inositol starvation. Suppression of this mutant for growth on glucose takes place by the loss of glucose 6-phosphate dehydrogenase. A lesion in the latter enzyme alone leaves growth practically unaffected. The mutations define the respective structural genes.

In VivoDynamics of the Pentose Phosphate Pathway inSaccharomyces cerevisiae

“…During this period, the cell accumulates intermediary metabolites of the ppp. Although the levels of the ppp fluxes decrease after this period, the slight differences between those become increasingly important, causing the instantaneous accumulation of R5P and E4P, as well as the degradation of the more toxic 6PG (Maitra et al 1982 …”

Mutants in Glucose Metabolism

“…Strains carrying gndJ did not grow on glucose, possibly because of 6-phosphogluconate accumula tion, secondary loss of glucose-6-P dehydrogenase (zwJl mutation) restoring growth. GND J and ZWFl are likely the structural genes, and single-gene zwJJ mutants were unaffected in their growth on glucose (176).…”

Targeted disruption of the housekeeping gene encoding glucose 6-phosphate dehydrogenase (G6PD): G6PD is dispensable for pentose synthesis but essential for defense against oxidative stress.

“…Diamide has little effect on the cloning efficiency of normal cells, but it causes a further dose-related reduction in the cloning efficiency of G6PD null cells (Figure 4). Hydrogen peroxide is probably the form of reactive oxygen to which cells are most commonly exposed in vivo (Cohen and Hochstein, 1964 Fraenkel, 1968) and yeast (Saccharomyces cerevisiae; Lobo and Maitra, 1982;Nogae and Johnston, 1990). In yeast, the mutation makes the cells auxotrophic for methionine by a mechanism that is still obscure (Thomas et al, 1991).…”