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水稻悬浮培养细胞中α-淀粉酶基因表达的代谢去阻遏作用

Metabolic derepression of alpha-amylase gene expression in suspension-cultured cells of rice.

作者信息

Yu S M, Kuo Y H, Sheu G, Sheu Y J, Liu L F

机构信息

Institute of Molecular Biology, Academia Sinica, Taipei, Taiwan, Republic of China.

出版信息

J Biol Chem. 1991 Nov 5;266(31):21131-7.

PMID:1939156
Abstract

We present evidence to show that the alpha-amylase gene family in rice is under two different modes of regulation: 1) hormonal regulation in germinating seeds, and 2) metabolic repression in cultured cells by available carbohydrate nutrients. Expression of alpha-amylase genes in deembryoed rice seeds is known to be induced by exogenous gibberellic acid. On the other hand, expression of alpha-amylase genes in suspension-cultured cells is induced by the deprivation of carbohydrate nutrient. A lag period of 2-4 h is required for the induction of alpha-amylase mRNA in sucrose-depleted medium. The induction of alpha-amylase expression is extraordinarily high and levels of alpha-amylase mRNA can be increased 8-20-folds after 24 h of sucrose starvation. The synthesis and secretion of alpha-amylase is also dependent upon the level of carbon source. The derepression or repression of alpha-amylase synthesis can be readily reversed by the deprivation or replenishment of sucrose in the medium, respectively. Glucose and fructose exert a repression on the alpha-amylase synthesis similar to that of sucrose. A hypothesis that explains the induction of alpha-amylase synthesis by carbohydrate starvation is proposed. Our data have suggested a hitherto undiscovered, potentially important control mechanism of carbohydrate metabolism in higher plants.

摘要

我们提供的证据表明,水稻中的α-淀粉酶基因家族受两种不同的调控模式影响:1)萌发种子中的激素调控,以及2)培养细胞中可利用碳水化合物营养物质的代谢抑制。已知去胚水稻种子中α-淀粉酶基因的表达受外源赤霉素诱导。另一方面,悬浮培养细胞中α-淀粉酶基因的表达受碳水化合物营养物质缺乏的诱导。在蔗糖耗尽的培养基中诱导α-淀粉酶mRNA需要2 - 4小时的延迟期。α-淀粉酶表达的诱导非常高,蔗糖饥饿24小时后α-淀粉酶mRNA水平可增加8 - 20倍。α-淀粉酶的合成和分泌也取决于碳源水平。培养基中蔗糖的缺乏或补充可分别轻易逆转α-淀粉酶合成的去抑制或抑制。葡萄糖和果糖对α-淀粉酶合成的抑制作用与蔗糖类似。提出了一个解释碳水化合物饥饿诱导α-淀粉酶合成的假说。我们的数据表明了高等植物中一种迄今未被发现的、潜在重要的碳水化合物代谢控制机制。

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