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Phosphite-mediated suppression of phosphate starvation responses in Arabidopsis
Shang Jye Leong
|關鍵字:||磷酸鹽;亞磷酸鹽;缺磷逆境;花青素;粒線體ATP生合成;醣類;缺磷反應之基因;防禦性基因;非PHR1之轉錄因子;phosphate;phosphite;phosphate starvation;anthocyanin;mitochondrial ATP synthesis;sugars;phosphate starvation responsive (PSR) genes;defense-related genes;non-PHR1 transcription factors||引用:||Achary, V.M.M., Ram, B., Manna, M., Datta, D., Bhatt, A., Reddy, M.K., et al. (2017) Phosphite: a novel P fertilizer for weed management and pathogen control. Plant Biotechnol. J. 15: 1493-1508. Adams, F. and Conrad, J.P. (1953) Transition of phosphite to phosphate in soils. Soil Science 75: 361-371. Agerbirk, N., De Vos, M., Kim, J.H. and Jander, G. (2008) Indole glucosinolate breakdown and its biological effects. Phytochem. Rev. 8: 101-120. Alexova, R., Nelson, C.J. and Millar, A.H. (2017) Temporal development of the barley leaf metabolic response to Pi limitation. Plant Cell Environ. 40: 645-657. Alford, S.R., Rangarajan, P., Williams, P. and Gillaspy, G.E. 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Despite the essential role of phosphate (Pi) in plant growth and development, how plants sense and signal the change of Pi supply to adjust its uptake and utilization is not yet well understood. Pi itself has been proposed to be a signaling molecule that regulates Pi starvation responses (PSRs) because phosphite (Phi), a non-metabolized Pi analog, suppresses several PSRs. Here, we exploit Phi to study the signaling and regulation of PSRs via two approaches, genetic screening of mutants under Phi treatment and transcriptomic analysis of short-term Phi application to Pi-starved plants. In the first approach, we identified a phosphite-insensitive1 (phi1) mutant which retained anthocyanin, a visible PSR, under Phi-containing but Pi-deficient medium. phi1 mutants were impaired in the gene encoding an FAd subunit of mitochondrial F1Fo-ATP synthase and showed reduced mitochondrial ATP level in roots, growth hypersensitivity to oligomycin and an increased mitochondrial membrane potential, suggesting that this gene has a crucial role in mitochondrial ATP synthesis. phi1 mutants accumulated a high level of sugars in shoots, which may account for the increased accumulation of anthocyanin and starch in Phi-containing conditions. Gene expression analysis showed that a subset of genes involved in carbohydrate metabolism in phi1 was mis-regulated in response to Phi. The majority of genes were repressed by Pi starvation and unlike wild-type plants, their repression in phi1 was not affected by the addition of Phi. Our findings show that defective mitochondrial ATP synthesis results in sugar accumulation, leading to alteration of Phi-mediated suppression of PSRs. This study reinforces the role of sugars, and also reveals a crosstalk among ATP, sugars and Pi/Phi molecules in mediating Pi signaling. In the second approach, we attempted to distinguish PSR genes directly regulated by Pi from those regulated by its metabolites. We found that majority of PSR genes were suppressed by both Pi and Phi, although a subset of PSR genes was less responsive to Phi. This suggests most of PSR genes are regulated by Pi itself rather than its metabolites. Intriguingly, we identified a subset of genes enriched in defense-related functions that showed opposite responses to Pi and Phi. Cis-element analysis of promoter sequences revealed the involvement of several candidates of transcriptional factors in addition to PHR1/PHL family proteins in regulating the expression of Pi-regulated PSR genes. Taken together, this study not only highlights the role of Pi as a signaling molecule, but provides information about other potential components or mechanisms in regulation of PSR genes, as well as additional effects of Phi on plants.
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