首页    期刊浏览 2024年12月04日 星期三
登录注册

文章基本信息

  • 标题:Defense gene induction in tobacco by nitric oxide, cyclic GMP, and cyclic ADP-ribose
  • 本地全文:下载
  • 作者:Jörg Durner ; David Wendehenne ; Daniel F. Klessig
  • 期刊名称:Proceedings of the National Academy of Sciences
  • 印刷版ISSN:0027-8424
  • 电子版ISSN:1091-6490
  • 出版年度:1998
  • 卷号:95
  • 期号:17
  • 页码:10328-10333
  • DOI:10.1073/pnas.95.17.10328
  • 语种:English
  • 出版社:The National Academy of Sciences of the United States of America
  • 摘要:Reactive oxygen species are believed to perform multiple roles during plant defense responses to microbial attack, acting in the initial defense and possibly as cellular signaling molecules. In animals, nitric oxide (NO) is an important redox-active signaling molecule. Here we show that infection of resistant, but not susceptible, tobacco with tobacco mosaic virus resulted in enhanced NO synthase (NOS) activity. Furthermore, administration of NO donors or recombinant mammalian NOS to tobacco plants or tobacco suspension cells triggered expression of the defense-related genes encoding pathogenesis-related 1 protein and phenylalanine ammonia lyase (PAL). These genes were also induced by cyclic GMP (cGMP) and cyclic ADP-ribose, two molecules that can serve as second messengers for NO signaling in mammals. Consistent with cGMP acting as a second messenger in tobacco, NO treatment induced dramatic and transient increases in endogenous cGMP levels. Furthermore, NO-induced activation of PAL was blocked by 6-anilino-5,8-quinolinedione and 1H-(1,2,4)-oxadiazole[4,3-a]quinoxalin-1-one, two inhibitors of guanylate cyclase. Although 6-anilino-5,8-quinolinedione fully blocked PAL activation, inhibition by 1H-(1,2,4)-oxadiazole[4,3-a]quinoxalin-1-one was not entirely complete, suggesting the existence of cGMP-independent, as well as cGMP-dependent, NO signaling. We conclude that several critical players of animal NO signaling are also operative in plants.
  • 关键词:reactive oxygen species/guanylate cyclase/pathogenesis-related proteins/calcium/plant signal transduction
国家哲学社会科学文献中心版权所有