The phenotype of the Arabidopsis cue1 mutant is not simply caused by a general restriction of the shikimate pathway

被引:81
作者
Voll, L
Häusler, RE
Hecker, R
Weber, A
Weissenböck, G
Fiene, G
Waffenschmidt, S
Flügge, UI
机构
[1] Univ Cologne, Inst Bot, D-50931 Cologne, Germany
[2] Univ Cologne, Inst Biochem, D-50674 Cologne, Germany
关键词
phenylpropanoids; secondary metabolism; phosphoenolpyruvate transport; aromatic amino acids; cue1; mutant; plastids;
D O I
10.1046/j.1365-313X.2003.01889.x
中图分类号
Q94 [植物学];
学科分类号
071001 ;
摘要
The Arabidopsis thaliana chlorophyll a/b binding protein underexpressed (cue1) mutant, which has been isolated in a screen for chlorophyll a/b binding protein (CAB) underexpressors, exhibits a reticulate leaf phenotype combined with delayed chloroplast development and aberrant shape of the palisade parenchyma cells. The affected gene in cue1 is a phosphoenolpyruvate (PEP)/phosphate translocator (PPT) of the plastid inner envelope membrane. The proposed function of the PPT in C-3-plants is the import of PEP into the stroma as one of the substrates for the shikimate pathway, from which aromatic amino acids and a variety of secondary plant products derive. The mutant phenotype could be: (i) complemented by constitutive overexpression of a heterologous PPT from cauliflower; and (ii) rescued by overexpression of a C-4-type pyruvate,orthophosphate dikinase (PPDK). The latter approach indicates that PEP deficiency within plastids triggers developmental constraints in cue1. The impact of the mutation on aspects of primary and secondary metabolism was assessed in cue1 as well as in the individual transformant lines. The majority of the data obtained in this and an accompanying paper suggest that the mutant phenotype is not simply caused by a general restriction of the shikimate pathway because of a defect in a PPT.
引用
收藏
页码:301 / 317
页数:17
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