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The rice OsERF101 transcription factor regulates the NLR Xa1‐mediated immunity induced by perception of TAL effectors
Author(s) -
Yoshihisa Ayaka,
Yoshimura Satomi,
Shimizu Motoki,
Sato Sayaka,
Matsuno Shogo,
Mine Akira,
Yamaguchi Koji,
Kawasaki Tsutomu
Publication year - 2022
Publication title -
new phytologist
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.742
H-Index - 244
eISSN - 1469-8137
pISSN - 0028-646X
DOI - 10.1111/nph.18439
Subject(s) - effector , biology , transcription factor , microbiology and biotechnology , xanthomonas oryzae , complementation , gene , mutant , genetics , gene knockout
Summary Plant nucleotide‐binding leucine‐rich repeat receptors (NLRs) initiate immune responses by recognizing pathogen effectors. The rice gene Xa1 encodes an NLR with an N‐terminal BED domain, and recognizes transcription activator‐like (TAL) effectors of Xanthomonas oryzae pv oryzae ( Xoo ). Our goal here was to elucidate the molecular mechanisms controlling the induction of immunity by Xa1. We used yeast two‐hybrid assays to screen for host factors that interact with Xa1 and identified the AP2/ERF‐type transcription factor OsERF101/OsRAP2.6. Molecular complementation assays were used to confirm the interactions among Xa1, OsERF101 and two TAL effectors. We created OsERF101 ‐overexpressing and knockout mutant lines in rice and identified genes differentially regulated in these lines, many of which are predicted to be involved in the regulation of response to stimulus. Xa1 interacts in the nucleus with the TAL effectors and OsERF101 via the BED domain. Unexpectedly, both the overexpression and the knockout lines of OsERF101 displayed Xa1‐dependent, enhanced resistance to an incompatible Xoo strain. Different sets of genes were up‐ or downregulated in the overexpression and knockout lines. Our results indicate that OsERF101 regulates the recognition of TAL effectors by Xa1, and functions as a positive regulator of Xa1‐mediated immunity. Furthermore, an additional Xa1‐mediated immune pathway is negatively regulated by OsERF101.