Department of Microbiology and Cell Science, University of Florida, PO Box 110700, Gainesville, FL 32611, USA.
Plant J. 2010 Nov;64(3):511-23. doi: 10.1111/j.1365-313X.2010.04345.x. Epub 2010 Sep 28.
Immune responses in eukaryotes involve rapid and profound transcriptional reprogramming. Although mechanisms regulating the amplitude of defense gene expression have been extensively characterized, those controlling the speed of defense gene induction are not well understood. Here, we show that the Arabidopsis Elongator subunit 2 (AtELP2) regulates the kinetics of defense gene induction. AtELP2 is required for rapid defense gene induction and the establishment of full basal and effector-triggered immunity (ETI). Surprisingly, biological or chemical induction of systemic acquired resistance (SAR), a long-lasting plant immunity against a broad spectrum of pathogens, restores pathogen resistance to Atelp2 mutant plants. Simultaneous removal of AtELP2 and NPR1, a transcription coactivator essential for full-scale expression of a subset of defense genes and the establishment of SAR, completely abolishes resistance to two different ETI-inducing pathogens. These results demonstrate that AtELP2 is an accelerator of defense gene induction, which functions largely independently of NPR1 in establishing plant immunity.
真核生物的免疫反应涉及快速而深刻的转录重编程。尽管已经广泛研究了调节防御基因表达幅度的机制,但控制防御基因诱导速度的机制尚不清楚。在这里,我们表明拟南芥延伸因子亚基 2(AtELP2)调节防御基因诱导的动力学。AtELP2 是快速防御基因诱导和完全建立基础和效应子触发免疫(ETI)所必需的。令人惊讶的是,系统性获得性抗性(SAR)的生物或化学诱导——一种针对广泛病原体的持久植物免疫——恢复了 Atelp2 突变体植物对病原体的抗性。同时去除 AtELP2 和 NPR1,NPR1 是一组防御基因和 SAR 建立的全规模表达所必需的转录共激活因子,完全消除了对两种不同 ETI 诱导病原体的抗性。这些结果表明,AtELP2 是防御基因诱导的加速器,它在建立植物免疫方面在很大程度上独立于 NPR1 发挥作用。