bZIP10-LSD1 antagonism modulates basal defense and cell death in Arabidopsis following infection

被引:199
作者
Kaminaka, Hironori
Naeke, Christian
Epple, Petra
Dittgen, Jan
Schuetze, Katia
Chaban, Christina
Holt, Ben F., III
Merkle, Thomas
Schaefer, Eberhard
Harter, Klaus
Dangl, Jeffery L.
机构
[1] Zentrum Mol Biol Pflanzen Pflanzenphysiol, D-72076 Tubingen, Germany
[2] Univ N Carolina, Dept Biol, Curriculum Genet, Chapel Hill, NC USA
[3] Univ N Carolina, Carolina Ctr Genome Sci, Chapel Hill, NC USA
[4] Tottori Univ, Fac Agr, Tottori 680, Japan
[5] Univ Freiburg, Inst Biol Bot 2, Freiburg, Germany
[6] Univ Bielefeld, Dept Genome Res, Ctr Biotechnol, D-4800 Bielefeld, Germany
[7] Univ N Carolina, Dept Microbiol & Immunol, Curriculum Genet, Chapel Hill, NC USA
关键词
basal defense; Hyaloperonospora parasitica; hypersensitive cell death; nuclear shuttling; reactive oxygen;
D O I
10.1038/sj.emboj.7601312
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 use sophisticated strategies to balance responses to oxidative stress. Programmed cell death, including the hypersensitive response (HR) associated with successful pathogen recognition, is one cellular response regulated by reactive oxygen in various cellular contexts. The Arabidopsis basic leucine zipper (bZIP) transcription factor AtbZIP10 shuttles between the nucleus and the cytoplasm and binds consensus G- and C-box DNA sequences. Surprisingly, AtbZIP10 can be retained outside the nucleus by LSD1, a protein that protects Arabidopsis cells from death in the face of oxidative stress signals. We demonstrate that AtbZIP10 is a positive mediator of the uncontrolled cell death observed in lsd1 mutants. AtbZIP10 and LSD1 act antagonistically in both pathogen-induced HR and basal defense responses. LSD1 likely functions as a cellular hub, where its interaction with AtbZIP10 and additional, as yet unidentified, proteins contributes significantly to plant oxidative stress responses.
引用
收藏
页码:4400 / 4411
页数:12
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