4.7 Article

Integrated metabolite and gene expression profiling revealing phytochrome A regulation of polyamine biosynthesis of Arabidopsis thaliana

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JOURNAL OF EXPERIMENTAL BOTANY
卷 59, 期 6, 页码 1187-1200

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OXFORD UNIV PRESS
DOI: 10.1093/jxb/ern026

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arabidopsis thaliana; gene expression pro. ling; metabolite pro. ling; phytochrome A; polyamine biosynthesis

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In this study, metabolite profiling was demonstrated as a useful tool to plot a specific metabolic pathway, which is regulated by phytochrome A (phyA). Etiolated Arabidopsis wild-type (WT) and phyA mutant seedlings were irradiated with either far-red light (FR) or white light (W). Primary metabolites of the irradiated seedlings were profiled by gas chromatography time-of-flight mass spectrometry (GC/TOF-MS) to obtain new insights on phyA-regulated metabolic pathways. Comparison of metabolite profiles in phyA and WT seedlings grown under FR revealed a number of metabolites that contribute to the differences between phyA and the WT. Several metabolites, including some amino acids, organic acids, and major sugars, as well as putrescine, were found in smaller amounts in WT compared with the content in phyA seedlings grown under FR. There were also significant differences between metabolite profiles of WT and phyA seedlings during de-etiolation under W. The polyamine biosynthetic pathway was investigated further, because putrescine, one of the polyamines existing in a wide variety of living organisms, was found to be present in lower amounts in WT than in phyA under both light conditions. The expression levels of polyamine biosynthesis-related genes were investigated by quantitative real-time RT-PCR. The gene expression profiles revealed that the arginine decarboxylase 2 (ADC2) gene was transcribed less in the WT than in phyA seedlings under both light conditions. This finding suggests that ADC2 is negatively regulated by phyA during photomorphogenesis. In addition, S-adenosylmethionine decarboxylase 2 and 4 (SAMDC2 and SAMDC4) were found to be regulated by phyA but in a different manner from the regulation of ADC2.

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