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

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作者
Rebecca Lyons
Akira Iwase
Thomas Gänsewig
Alexander Sherstnev
Céline Duc
Geoffrey J. Barton
Kousuke Hanada
Mieko Higuchi-Takeuchi
Minami Matsui
Keiko Sugimoto
Kemal Kazan
Gordon G. Simpson
Ken Shirasu
机构
[1] RIKEN Plant Science Center,Frontier Research Academy for Young Researchers, Department of Bioscience and Bioinformatics
[2] Tsurumi-ku,undefined
[3] Commonwealth Scientific and Industrial Research Organization Plant Industry,undefined
[4] Queensland Bioscience Precinct,undefined
[5] RIKEN Center for Sustainable Resource Science,undefined
[6] Tsurumi-ku,undefined
[7] College of Life Sciences,undefined
[8] University of Dundee,undefined
[9] Kyushu Institute of Technology,undefined
[10] James Hutton Institute,undefined
[11] Invergowrie,undefined
来源
Scientific Reports | / 3卷
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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.
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