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bZIP10与LSD1的拮抗作用在拟南芥感染后调节基础防御和细胞死亡。

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

作者信息

Kaminaka Hironori, Näke Christian, Epple Petra, Dittgen Jan, Schütze Katia, Chaban Christina, Holt Ben F, Merkle Thomas, Schäfer Eberhard, Harter Klaus, Dangl Jeffery L

机构信息

Department of Biology, Curriculum in Genetics and Carolina Center for Genome Sciences, CB#3280, University of North Carolina, Chapel Hill, NC 27599, USA.

出版信息

EMBO J. 2006 Sep 20;25(18):4400-11. doi: 10.1038/sj.emboj.7601312. Epub 2006 Sep 7.

Abstract

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.

摘要

植物运用复杂的策略来平衡对氧化应激的反应。程序性细胞死亡,包括与成功识别病原体相关的超敏反应(HR),是在各种细胞环境中由活性氧调节的一种细胞反应。拟南芥碱性亮氨酸拉链(bZIP)转录因子AtbZIP10在细胞核和细胞质之间穿梭,并结合共有G盒和C盒DNA序列。令人惊讶的是,AtbZIP10可以被LSD1保留在细胞核外,LSD1是一种在面对氧化应激信号时保护拟南芥细胞免于死亡的蛋白质。我们证明AtbZIP10是在lsd1突变体中观察到的不受控制的细胞死亡的正向介导因子。AtbZIP10和LSD1在病原体诱导的HR和基础防御反应中均起拮抗作用。LSD1可能作为一个细胞枢纽发挥作用,其与AtbZIP10以及其他尚未鉴定的蛋白质的相互作用对植物氧化应激反应有显著贡献。

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