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Saccharomyces cerevisiae mutants defective in the structural gene R i l l lack phosphoglucose isomerase and hence cannot grow on glucose. Spontaneous mutants were isolated by selecting for the regained ability to grow on YEPD (yeast extract/peptone/g I ucose). Three complementat ion groups ca I led spg29-31 (yuppressor of pgild) were identified. The metabolism of [2-13C]glucose was studiedby 13C NMR spectroscopy. This led to the conclusion that in a spg29 mutant suppression of the glycolytic defect was achieved by increased carbon flux through the hexose monophosphate pathway. The specific activities of enzymes of the hexose monophosphate pathway (except glucose-6-phosphate dehydrogenase) and NAD-and NADP-dependent glutamate dehydrogenase were increased in the bypass mutant.

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USELAT identified serogroups for 80% of samples, whereas LATs identified only 40%. The USELAT detection of the A, C, Y, and W135 antigen serogroups showed comparable enhancement for the kits tested. The commercial availability of latex beads coated with antibody to the Y and W135 serogroups would expedite their identification.