The RNA-binding protein FPA regulates flg22-triggered defense responses and transcription factor activity by alternative polyadenylation

被引:49
|
作者
Lyons, Rebecca [1 ,2 ]
Iwase, Akira [1 ,3 ]
Gansewig, Thomas [1 ]
Sherstnev, Alexander [4 ]
Duc, Celine [4 ]
Barton, Geoffrey J. [4 ]
Hanada, Kousuke [1 ,5 ]
Higuchi-Takeuchi, Mieko [1 ]
Matsui, Minami [1 ]
Sugimoto, Keiko [1 ,3 ]
Kazan, Kemal [2 ]
Simpson, Gordon G. [4 ,6 ]
Shirasu, Ken [1 ,3 ]
机构
[1] RIKEN, Plant Sci Ctr, Tsurumi Ku, Yokohama, Kanagawa 2300045, Japan
[2] Queensland Biosci Precinct, Commonwealth Sci & Ind Res Org Plant Ind, St Lucia, Qld 4067, Australia
[3] RIKEN, Ctr Sustainable Resource Sci, Tsurumi Ku, Yokohama, Kanagawa 2300045, Japan
[4] Univ Dundee, Coll Life Sci, Dundee DD1 4HN, Scotland
[5] Kyushu Inst Technol, Frontier Res Acad Young Researchers, Dept Biosci & Bioinformat, Iizuka, Fukuoka 8208502, Japan
[6] James Hutton Inst, Dundee DD2 5DA, Scotland
来源
SCIENTIFIC REPORTS | 2013年 / 3卷
基金
英国生物技术与生命科学研究理事会;
关键词
ARABIDOPSIS-THALIANA; DISEASE RESISTANCE; FLOWERING-TIME; ABSCISIC-ACID; III EFFECTOR; E3; LIGASE; PLANT; ETHYLENE; REPRESSOR; IMMUNITY;
D O I
10.1038/srep02866
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
RNA-binding proteins (RBPs) play an important role in plant host-microbe interactions. In this study, we show that the plant RBP known as FPA, which regulates 3'-end mRNA polyadenylation, negatively regulates basal resistance to bacterial pathogen Pseudomonas syringae in Arabidopsis. A custom microarray analysis reveals that flg22, a peptide derived from bacterial flagellins, induces expression of alternatively polyadenylated isoforms of mRNA encoding the defence-related transcriptional repressor ETHYLENE RESPONSE FACTOR 4 (ERF4), which is regulated by FPA. Flg22 induces expression of a novel isoform of ERF4 that lacks the ERF-associated amphiphilic repression (EAR) motif, while FPA inhibits this induction. The EAR-lacking isoform of ERF4 acts as a transcriptional activator in vivo and suppresses the flg22-dependent reactive oxygen species burst. We propose that FPA controls use of proximal polyadenylation sites of ERF4, which quantitatively limit the defence response output.
引用
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页数:10
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