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Arachidonic acid alters tomato HMG expression and fruit growth and induces 3-hydroxy-3-methylglutaryl coenzyme A reductase-independent lycopene accumulation

机译:花生四烯酸改变番茄HMG表达和果实生长并诱导3-羟基-3-甲基戊二酰辅酶A不依赖还原酶的番茄红素积累

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摘要

Regulation of isoprenoid end-product synthesis required for normal growth and development in plants is not well understood. To investigate the extent to which specific genes for the enzyme 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGR) are involved in end-product regulation, we manipulated expression of the HMG1 and HMG2 genes in tomato (Lycopersicon esculentum) fruit using arachidonic acid (AA). In developing young fruit AA blocked fruit growth, inhibited HMG1, and activated HMG2 expression. These results are consistent with other reports indicating that HMG1 expression is closely correlated with growth processes requiring phytosterol production. In mature-green fruit AA strongly induced the expression of HMG2, PSY1 (the gene for phytoene synthase), and lycopene accumulation before the normal onset of carotenoid synthesis and ripening. The induction of lycopene synthesis was not blocked by inhibition of HMGR activity using mevinolin, suggesting that cytoplasmic HMGR is not required for carotenoid synthesis. Our results are consistent with the function of an alternative plastid isoprenoid pathway (the Rohmer pathway) that appears to direct the production of carotenoids during tomato fruit ripening.
机译:植物中正常生长和发育所需的类异戊二烯终产物合成的调控尚不清楚。若要调查3-羟基-3-甲基戊二酰辅酶A还原酶(HMGR)的特定基因参与最终产品调节的程度,我们使用花生四烯酸操纵了番茄(番茄)中HMG1和HMG2基因的表达酸(AA)。在发育年轻果实中,AA阻止果实生长,抑制HMG1,并激活HMG2表达。这些结果与其他报告一致,表明HMG1表达与需要植物甾醇生成的生长过程密切相关。在成熟的绿色水果中,AA在类胡萝卜素合成和成熟的正常发作之前强烈诱导HMG2,PSY1(植物四烯合酶的基因)和番茄红素的表达。番茄红素合成的诱导并没有通过使用米维诺林抑制HMGR活性而被阻止,这表明类胡萝卜素合成不需要细胞质HMGR。我们的结果与替代质体类异戊二烯途径(Rohmer途径)的功能一致,该途径似乎指导番茄果实成熟过程中类胡萝卜素的产生。

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