Six-day-old, dark-grown, seedlings of barley homozygous for the recessive mutationtigrina d12accumulated 5-aminolevulinic acid (ALA) and protochlorophyll (ide) in amounts exceeding the wild type level. Transferring the etiolated mutant to light resulted in the destruction of pigments and the deterioration of the ALA forming system. Such deleterious effects did not occurusing light-grown mutant or etiolated and greened wild type seedlings. Gabaculine (GAB) at 50μM inhibited ALA synthesis by about 85when etiolated wild type seedlings were exposed to light. In light-grown leaves of either wild type or mutant strain, ALA production was also sharply (ca. 75) inhibited by GAB. During dark incubation, however, the inhibition of ALA accumulation did not exceed 50in all types of tissues. The results give further evidence for the operation of the C5pathway in such seedlings since GAB decreased the biosynthesis of ALA to the same extent in bothtigrina d12mutant and wild type of barley
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