2020年2月
Regulation of Sugar and Storage Oil Metabolism by Phytochrome during De-etiolation
Plant Physiology
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- 巻
- 182
- 号
- 2
- 開始ページ
- 1114
- 終了ページ
- 1129
- 記述言語
- 英語
- 掲載種別
- 研究論文(学術雑誌)
- DOI
- 10.1104/pp.19.00535
- 出版者・発行元
- Oxford University Press (OUP)
Exposure of dark-grown (etiolated) seedlings to light induces the heterotrophic-to-photoautotrophic transition (de-etiolation) processes, including the formation of photosynthetic machinery in the chloroplast and cotyledon expansion. Phytochrome is a red (R)/far-red (FR) light photoreceptor that is involved in the various aspects of de-etiolation. However, how phytochrome regulates metabolic dynamics in response to light stimulus has remained largely unknown. In this study, to elucidate the involvement of phytochrome in the metabolic response during de-etiolation, we performed widely targeted metabolomics in Arabidopsis (Arabidopsis thaliana) wild-type and phytochrome A and B double mutant seedlings de-etiolated under R or FR light. The results revealed that phytochrome had strong impacts on the primary and secondary metabolism during the first 24 h of de-etiolation. Among those metabolites, sugar levels decreased during de-etiolation in a phytochrome-dependent manner. At the same time, phytochrome upregulated processes requiring sugars. Triacylglycerols are stored in the oil bodies as a source of sugars in Arabidopsis seedlings. Sugars are provided from triacylglycerols through fatty acid β-oxidation and the glyoxylate cycle in glyoxysomes. We examined if and how phytochrome regulates sugar production from oil bodies. Irradiation of the etiolated seedlings with R and FR light dramatically accelerated oil body mobilization in a phytochrome-dependent manner. Glyoxylate cycle-deficient mutants not only failed to mobilize oil bodies but also failed to develop thylakoid membranes and expand cotyledon cells upon exposure to light. Hence, phytochrome plays a key role in the regulation of metabolism during de-etiolation.
- リンク情報
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- DOI
- https://doi.org/10.1104/pp.19.00535
- PubMed
- https://www.ncbi.nlm.nih.gov/pubmed/31748417
- PubMed Central
- https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6997681
- Web of Science
- https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000513631100033&DestApp=WOS_CPL
- URL
- https://syndication.highwire.org/content/doi/10.1104/pp.19.00535
- ID情報
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- DOI : 10.1104/pp.19.00535
- ISSN : 0032-0889
- eISSN : 1532-2548
- PubMed ID : 31748417
- PubMed Central 記事ID : PMC6997681
- Web of Science ID : WOS:000513631100033