4.6 Article

MYB96-mediated abscisic acid signals induce pathogen resistance response by promoting salicylic acid biosynthesis in Arabidopsis

期刊

NEW PHYTOLOGIST
卷 186, 期 2, 页码 471-483

出版社

WILEY
DOI: 10.1111/j.1469-8137.2010.03183.x

关键词

abscisic acid; Arabidopsis; disease resistance; MYB96; salicylic acid; SID2

资金

  1. Brain Korea 21
  2. Biogreen 21 [20080401034001]
  3. National Research Laboratory programs
  4. Plant Signaling Network Research Center [2009-0079297]
  5. Korea Science and Engineering Foundation [2007-03415]
  6. Agricultural R& D Promotion Center [309017-5]
  7. Korea Ministry for Food, Agriculture, Forestry and Fisheries

向作者/读者索取更多资源

The Arabidopsis MYB96 transcription factor plays a role in abscisic acid (ABA)-mediated drought response. Notably, anthocyanins accumulate in the activation-tagging myb96-1d line, suggesting a role of MYB96 in biotic and abiotic stress responses in plants. Here, we investigate the role of MYB96 in salicylic acid (SA) biosynthesis and plant defense and explore the mechanisms underlying the ABA-SA interaction. myb96-1d and myb96-1 were subject to pathogen infection assays, and expression of SA biosynthetic and defense genes was examined. myb96-1d was crossed with the NahG transgenic plants to investigate the role of MYB96 in ABA regulation of SA biosynthesis. Whereas myb96-1d exhibited an enhanced disease resistance, myb96-1 was susceptible to pathogen infection. A subset of pathogenesis-related (PR) genes was up-regulated in myb96-1d. However, PR transcript abundances were reduced in myb96-1d X NahG. Interestingly, a SA biosynthetic gene SALICYLIC ACID INDUCTION DEFICIENT2 (SID2) was up-regulated, and concentrations of SA and SA-beta-glucoside (SAG) were elevated in myb96-1d. In addition, the inductive effects of abiotic stresses on SID2 were reduced in aba3-1. Our observations indicate that MYB96-mediated ABA signals enhance plant disease resistance by inducing SA biosynthesis. It is envisioned that MYB96 is a molecular link that mediates ABA-SA crosstalks.

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