Genome-wide analyses of direct target genes of an ERF11 transcription factor involved in plant defense against bacterial pathogens

被引:10
作者
Wu, Juan [1 ,2 ]
Deng, Yong [1 ]
Hu, Junhe [2 ]
Jin, Chenzhong [2 ]
Zhu, Xiwu [2 ]
Li, Defang [1 ]
机构
[1] Chinese Acad Agr Sci, Inst Bast Fiber Crops, Changsha 410205, Peoples R China
[2] Hunan Univ Humanities Sci & Technol, Inst Agr & Biotechnol, Loudi 41700, Peoples R China
关键词
ERF11; ChIP-seq; Bacterial pathogens; NIMIN2; TAF15b; ERF4; DISEASE RESISTANCE; CELL-DEATH; CHIP-SEQ; ARABIDOPSIS; OVEREXPRESSION; PROTEINS; NPR1; BIOSYNTHESIS; INDUCTION; REPRESSOR;
D O I
10.1016/j.bbrc.2020.07.073
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
Ethylene responsive factor ERF11 containing the ERF-associated amphiphilic repression (EAR) motif enhances plant resistance to bacterial pathogens. However, the underlying molecular mechanisms regulated by transcription factor ERF11 are poorly understood, in tobacco or other model plants. Here, we revealed the genome-wide binding landscape of BrERF11b in Nicotiana benthamian by conducting chromatin immunoprecipitation experiments followed by high-throughput sequencing (ChIP-seq) and bioinformatic analyses. Our results also revealed a GCCbox-like consensus BrERF11b-binding DNA motif: VCGCCGCC. By further integrative analysis of ChIP-seq and RNA-seq data, and the confirmation of electrophoretic mobility shift assay (EMSA), we screened three direct target genes NbNIMIN2, NbTAF15b and NbERF4. These results suggest that ERF11 may be involved in NPR1-mediated systemic acquired resistance (SAR), nucleotide-binding leucine-rich repeat immune receptors (NLR) -mediated autoimmunity, and H2O2 generation, by direct transcriptional repression of NIM1-INTERACTING2 (NIMIN2), and transcriptional activation of TATA-binding protein-associated factor 15b (TAF15b) and ERF4. Our findings provide insightful information and valuable gene resource in unraveling the regulatory networks of plant defense responses to bacterial pathogens. (C) 2020 Elsevier Inc. All rights reserved.
引用
收藏
页码:76 / 81
页数:6
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