Six-day-old, dark-grown, seedlings of barley homozygous for the recessive mutation tigrina d12 accumulated 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 occur using light-grown mutant or etiolated and greened wild type seedlings. Gabaculine (GAB) at 50-mu-M inhibited ALA synthesis by about 85% when 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 50% in all types of tissues. The results give further evidence for the operation of the C5 pathway in such seedlings since GAB decreased the biosynthesis of ALA to the same extent in both tigrina d12 mutant and wild type of barley.