Abstract
Phosphoenolpyruvate (PEP) serves not only as a high energy carbon compound in glycolysis, but it acts also as precursor for plastidial anabolic sequences like the shikimate pathway, which produces aromatic amino acids (AAA) and subsequently secondary plant products. After conversion to pyruvate, PEP can also enter de novo fatty acid biosynthesis, the synthesis of branched-chain amino acids, and the non-mevalonate way of isoprenoid production. As PEP cannot be generated by glycolysis in chloroplasts and a variety of non-green plastids, it has to be imported from the cytosol by a phosphate translocator (PT) specific for PEP (PPT). A loss of function of PPT1 in Arabidopsis thaliana results in the chlorophyll a/b binding protein underexpressed1 (cue1) mutant, which is characterized by reticulate leaves and stunted roots. Here we dissect the shoot- and root phenotypes, and also address the question whether or not long distance signaling by metabolites is involved in the perturbed mesophyll development of cue1. Reverse grafting experiments showed that the shoot- and root phenotypes develop independently from each other, ruling out long distance metabolite signaling. The leaf phenotype could be transiently modified even in mature leaves, e.g. by an inducible PPT1RNAi approach or by feeding AAA, the cytokinin trans-zeatin (tZ), or the putative signaling molecule dehydrodiconiferyl alcohol glucoside (DCG). Hormones, such as auxins, abscisic acid, gibberellic acid, ethylene, methyl jasmonate, and salicylic acid did not rescue the cue1 leaf phenotype. The low cell density1 (lcd1) mutant shares the reticulate leaf-, but not the stunted root phenotype with cue1. It could neither be rescued by AAA nor by tZ. In contrast, tZ and AAA further inhibited root growth both in cue1 and wild-type plants. Based on our results, we propose a model that PPT1 acts as a net importer of PEP into chloroplast, but as an overflow valve and hence exporter in root plastids.
Highlights
The Arabidopsis thaliana cue1 mutant has been isolated almost 20 years ago in a screen for mutants defective in light-triggered activation of gene expression during germination (Li et al, 1995)
THE cue1 MUTANTS SHOWS AT LEAST FOUR SEPARATE SUB-PHENOTYPES AND SHARES ONLY RETICULATE LEAVES WITH THE lcd1 MUTANT The deficiency in PPT1 results in a complex phenotype of the cue1 mutant alleles, which can be divided into four separate sub-phenotypes
These are (i) growth retardation of the shoot (Figures 1D,F) compared to the control or wild-type plants, (ii) a reticulate leaf structure based on smaller mesophyll cells and chloroplasts therein. (iii) More pronounced serrations at the margins of the leaves lead to an altered overall leaf shape
Summary
The Arabidopsis thaliana cue mutant has been isolated almost 20 years ago in a screen for mutants defective in light-triggered activation of gene expression during germination (Li et al, 1995). The phosphoenolpyruvate (PEP)/PT (Fischer et al, 1997) defective in cue belongs, together with the triose phosphate/PT (TPT; Flügge et al, 1989), the glucose 6-P/PT (GPT; Kammerer et al, 1998), and the xylulose 5-P/PT (XPT; Eicks et al, 2002) to the PT gene family (Knappe et al, 2003a). Impaired PEP transport in plastids provision of PEP for the shikimate pathway (Fischer et al, 1997), which is entirely localized in the plastid stroma (Herrmann, 1995; Schmid and Amrhein, 1995; Herrmann and Weaver, 1999). In C4 and Crassulaceen acid metabolism (CAM) plants the PPT acts as net PEP exporter from the chloroplasts. During C4 photosynthesis and CAM, PEP is synthesized from pyruvate in the mesophyll chloroplasts by pyruvate:phosphate dikinase (PPDK) and has to be exported to the cytosol, where PEP carboxylase, the starting point of the C4 cycle or CAM, is localized (e.g., Häusler et al, 2000; Langdale, 2011)
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