Abstract
Detached fruits of the “lutescent”, high-beta and ghost tomatoes were treated with either dimethyl sulfoxide (DMSO) or 2-(4-chlorophenyl-thio)-triethylamine hydrochloride (CPTA) to study the biosynthetic origin of β-carotene in the tomato fruit. When mature “lutescent” tomato fruits (Stage 3) were treated with DMSO the synthesis of the acyclic carotenoids phytoene, phytofluene, ζ-carotene and lypocene was inhibited; the synthesis of β-carotene and the other cyclic carotenes was not affected. In less mature fruits (Stage 2), however, DMSO treatment inhibited synthesis of both acyclic and cyclic carotenoids. The synthesis of all the carotenoid fractions in high-beta fruits treated with DMSO at the mature green stage was inhibited. The high-beta fruit was found to contain increased levels of β-zeacarotene. Its synthesis, along with that of γ- and β-carotenes, decreased in the presence of DMSO. It was concluded-therefore-that the β-carotene fraction formed during ripening of the high-beta fruit is probably formed by cyclization of neurosporene to β-zeacarotene and not by cyclization of lypocene. It was suggested that the B+B,moB+moB genes probably control the balance between lypocene and β-carotene synthesis via a repressor-effector molecule interaction. Total carotenoid accumulation in ripened “lutescent” and high-beta tomato fruits was reduced by DMSO treatment. CPTA did not affect carotenogenesis in the ghost tomato mutant. The results suggest that CPTA can exert its influence only in an already existing pathway and will not overcome inhibition imposed by genetic mutation. The results suggest that CPTA can exert its influence only in an already existing pathway and will not overcome inhibition imposed by genetic mutation. In contrast, lypocene content increased fifteen-fold in the high-beta fruit treated with CPTA. The increase in the lypocene concentration was accompanied by a general increase in the level of the other acyclic carotenoids in the fruit. The β-zeacarotene, γ-carotene and β-carotene contents of the fruit decreased concomitantly. Total carotenoid accumulation in the high-beta fruit was reduced by CPTA. A re-evaluation of the results of earlier work on the genetics of the inheritance of tomato fruit color and tomato plastid structural studies in conjunction with the findings in this study indicate that (1) the additional level of β-carotene in the high-beta fruit may be formed mainly via the β-zeacarotene route, (2) the chloroplast β-carotene is probably produced through a biosynthetically independent pathway from the carotenes of chromoplast, and (3) the additional β-carotene fraction synthesized during ripening of the normal red tomato genotype is probably formed by a “carry-over” pathway
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