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胞质核糖-5-磷酸异构酶缺乏会导致拟南芥叶绿体功能障碍、开花延迟和细胞过早死亡。

Deficiency in a cytosolic ribose-5-phosphate isomerase causes chloroplast dysfunction, late flowering and premature cell death in Arabidopsis.

作者信息

Xiong Yuqing, DeFraia Christopher, Williams Donna, Zhang Xudong, Mou Zhonglin

机构信息

Department of Microbiology and Cell Science, University of Florida, Gainesville, FL 32611, USA.

出版信息

Physiol Plant. 2009 Nov;137(3):249-63. doi: 10.1111/j.1399-3054.2009.01276.x. Epub 2009 Aug 12.

DOI:10.1111/j.1399-3054.2009.01276.x
PMID:19744161
Abstract

The oxidative pentose phosphate pathway (oxPPP) is part of central metabolism, consisting of two distinct phases: the oxidative phase and the non-oxidative phase. The non-oxidative phase of the oxPPP generates carbon skeletons for the synthesis of nucleotides, aromatic amino acids, phenylpropanoids and their derivatives, which are essential for plant growth and development. However, it is not well understood how the non-oxidative phase of the oxPPP contributes to plant growth and development. Here, we report the characterization of Arabidopsis T-DNA knockout mutants of the RPI2 gene (At2g01290), which encodes a cytosolic ribose-5-phosphate isomerase (RPI) that catalyzes the reversible interconversion of ribulose-5-phosphate and ribose-5-phosphate in the non-oxidative phase of the oxPPP. Although recombinant Arabidopsis RPI2 protein exhibits marked RPI enzymatic activity, knockout of the RPI2 gene does not significantly change the total RPI activity in the mutant plants. Interestingly, knockout of RPI2 interferes with chloroplast structure and decreases chloroplast photosynthetic capacity. The rpi2 mutants accumulate less starch in the leaves and flower significantly later than wild-type when grown under short-day conditions. Furthermore, the rpi2 mutants display premature cell death in the leaves when grown at an above-normal temperature (26 degrees C). These results demonstrate that a deficiency in the non-oxidative phase of the cytosolic oxPPP has pleiotropic effects on plant growth and development and causes premature cell death.

摘要

氧化戊糖磷酸途径(oxPPP)是中心代谢的一部分,由两个不同阶段组成:氧化阶段和非氧化阶段。oxPPP的非氧化阶段产生用于合成核苷酸、芳香族氨基酸、苯丙烷类及其衍生物的碳骨架,这些对于植物生长发育至关重要。然而,目前尚不清楚oxPPP的非氧化阶段如何促进植物生长发育。在此,我们报道了拟南芥RPI2基因(At2g01290)T-DNA敲除突变体的特征,该基因编码一种胞质核糖-5-磷酸异构酶(RPI),在oxPPP的非氧化阶段催化核糖-5-磷酸和核酮糖-5-磷酸的可逆相互转化。尽管重组拟南芥RPI2蛋白表现出显著的RPI酶活性,但RPI2基因的敲除并未显著改变突变体植株中的总RPI活性。有趣的是,RPI2的敲除会干扰叶绿体结构并降低叶绿体光合能力。在短日条件下生长时,rpi2突变体叶片中积累的淀粉较少,开花时间比野生型显著延迟。此外,当在高于正常温度(26摄氏度)下生长时,rpi2突变体叶片中会出现过早的细胞死亡。这些结果表明,胞质oxPPP非氧化阶段的缺陷对植物生长发育具有多效性影响,并导致过早的细胞死亡。

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