Regulation of gene expression by jasmonate hormones

被引:129
作者
Memelink, Johan [1 ]
机构
[1] Leiden Univ, Inst Biol, Sylvius Lab, NL-2300 RA Leiden, Netherlands
关键词
Arabidopsis; AtMYC2; Catharanthus roseus; COI1; G-box; JAZ; Nicotine; ORA59; ORCA3; Promoter; SIGNAL-TRANSDUCTION PATHWAYS; N-METHYLTRANSFERASE GENES; BOX PROTEIN TIR1; METHYL-JASMONATE; TRANSCRIPTION FACTOR; SALICYLIC-ACID; ARABIDOPSIS-THALIANA; RESPONSIVE ELEMENT; DEFENSE RESPONSES; GCC-BOX;
D O I
10.1016/j.phytochem.2009.09.004
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Plants possess inducible defense systems to oppose attack by pathogens and herbivores. Jasmonates are important signaling molecules produced by plants which regulate in positive or negative crosstalk with ethylene subsets of genes involved in defense against necrotrophic microorganisms or herbivorous insects, respectively. This review presents an overview of promoter sequences and transcription factors involved in jasmonate-responsive gene expression with the most important components summarized here. Frequently occurring jasmonate-responsive promoter sequences are the GCC motif, which is commonly found in promoters activated synergistically by jasmonate and ethylene, and the G-box, which is commonly found in promoters activated by jasmonates and repressed by ethylene. Important transcription factors conferring jasmonate-responsive gene expression in Arabidopsis are ORA59 and AtMYC2. ORA59 interacts with the GCC motif and controls the expression of genes that are synergistically induced by jasmonates and ethylene, whereas AtMYC2 interacts with the G-box and related sequences, and controls genes activated by jasmonate alone. AtMYC2 can interact with JAZ proteins, which are hypothesized to act as repressors. The bioactive jasmonate (+)-7-iso-JA-L-Ile promotes the interaction between the ubiquitin ligase complex SCFCOI1 and JAZ proteins, resulting in their degradation by the 26S proteasome, thereby liberating AtMYC2 from repression according to the prevailing model. Literature up to 1 June 2009 was used for this review. (c) 2009 Elsevier Ltd. All rights reserved.
引用
收藏
页码:1560 / 1570
页数:11
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