論文

査読有り 国際誌
2020年9月27日

CLE2 regulates light-dependent carbohydrate metabolism in Arabidopsis shoots.

Plant molecular biology
  • Dichao Ma
  • ,
  • Satoshi Endo
  • ,
  • Shigeyuki Betsuyaku
  • ,
  • Akie Shimotohno
  • ,
  • Hiroo Fukuda

104
6
開始ページ
561
終了ページ
574
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1007/s11103-020-01059-y

KEY MESSAGE: This study focused on the role of CLE1-CLE7 peptides as environmental mediators and indicated that root-induced CLE2 functions systemically in light-dependent carbohydrate metabolism in shoots. Plants sense environmental stimuli and convert them into cellular signals, which are transmitted to distinct cells and tissues to induce adequate responses. Plant hormones and small secretory peptides often function as environmental stress mediators. In this study, we investigated whether CLAVATA3/EMBRYO SURROUNDING REGION-RELATED proteins, CLE1-CLE7, which share closely related CLE domains, mediate environmental stimuli in Arabidopsis thaliana. Expression analysis of CLE1-CLE7 revealed that these genes respond to different environmental stimuli, such as nitrogen deprivation, nitrogen replenishment, cold, salt, dark, and sugar starvation, in a sophisticated manner. To further investigate the function of CLE2, we generated transgenic Arabidopsis lines expressing the β-glucuronidase gene under the control of the CLE2 promoter or expressing the CLE2 gene under the control of an estradiol-inducible promoter. We also generated cle2-1 and cle2-2 mutants using the CRISPR/Cas9 technology. In these transgenic lines, dark induced the expression of CLE2 in the root vasculature. Additionally, induction of CLE2 in roots induced the expression of various genes not only in roots but also in shoots, and genes related to light-dependent carbohydrate metabolism were particularly induced in shoots. In addition, cle2 mutant plants showed chlorosis when subjected to a shade treatment. These results suggest that root-induced CLE2 functions systemically in light-dependent carbohydrate metabolism in shoots.

リンク情報
DOI
https://doi.org/10.1007/s11103-020-01059-y
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/32980951
ID情報
  • DOI : 10.1007/s11103-020-01059-y
  • PubMed ID : 32980951

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