C nuclear magnetic resonance (NMR) spectroscopy was used to study the metabolism of [2-C]acetate in a diploid strain of homozygous for the mutation. This mutation results in failure to initiate sporulation and suppresses mutations (which cause derepressed sporulation). By analysing the pattern of C-labelling in glutamate it was deduced that the glyoxylate cycle is responsible for most of the acetate utilization and that there is very little tricarboxylic acid cycle activity. The labelling of α,trehalose indicated that gluconeogenesis and the hexose monophosphate pathway operate in a similar way to the wild-type. The mutant strain has higher levels of succinate dehydrogenase than the wild-type. All of the physiological alterations caused by the mutation can be explained by this difference.


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