論文

査読有り
2004年3月

dwarf and delayed-flowering 1, a novel Arabidopsis mutant deficient in gibberellin biosynthesis because of overexpression of a putative AP2 transcription factor

PLANT JOURNAL
  • H Magome
  • ,
  • S Yamaguchi
  • ,
  • A Hanada
  • ,
  • Y Kamiya
  • ,
  • K Oda

37
5
開始ページ
720
終了ページ
729
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1111/j.1365-313X.2003.01998.x
出版者・発行元
BLACKWELL PUBLISHING LTD

A novel gibberellin (GA)-deficient mutant designated dwarf and delayed-flowering 1 (ddf1) was isolated from a library of activation-tagged Arabidopsis. This mutant showed dwarfism and late-flowering, but the phenotype was rescued by exogenous GA(3) like known mutants defective in GA biosynthesis. The contents of bioactive GA(4) and GA(1) were in fact decreased in ddf1 at least partially through the repression of biosynthetic steps catalyzed by GA 20-oxidase (GA20ox). Genetic and molecular analyses revealed that the ddf1 phenotypes are caused by increased or ectopic expression of a putative AP2 transcription factor. Overexpression of DDF2, encoding another putative AP2 transcription factor closely related to DDF1, also conferred the ddf1-like phenotype. Among genes encoding (putative) AP2 transcription factors in Arabidopsis, DDFs are phylogenetically close to dehydration-responsive element binding protein (DREB1)/C-repeat binding factor (CBF) genes, which are known to be involved in stress responses. The ddf1 mutation upregulates a stress-related gene RD29A. DDF1 mRNA is strongly induced by high-salinity stress within 1 h. Moreover, transgenic plants overexpressing DDF1 showed increased tolerance to high-salinity stress. These results suggest that DDF1 is involved in the regulation of GA biosynthesis and stress tolerance. The possible relation between the contents of endogenous GAs and acquisition of stress protection is discussed.

リンク情報
DOI
https://doi.org/10.1111/j.1365-313X.2003.01998.x
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/14871311
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000188865200007&DestApp=WOS_CPL
ID情報
  • DOI : 10.1111/j.1365-313X.2003.01998.x
  • ISSN : 0960-7412
  • PubMed ID : 14871311
  • Web of Science ID : WOS:000188865200007

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