National Institute of Science and Technology in Plant-Pest Interactions , Universidade Federal de Viçosa, 36570.000, Viçosa, Minas Gerais, Brazil.
Plant Physiol. 2014 Feb;164(2):654-70. doi: 10.1104/pp.113.231928. Epub 2013 Dec 6.
The binding protein (BiP) has been demonstrated to participate in innate immunity and attenuate endoplasmic reticulum- and osmotic stress-induced cell death. Here, we employed transgenic plants with manipulated levels of BiP to assess whether BiP also controlled developmental and hypersensitive programmed cell death (PCD). Under normal conditions, the BiP-induced transcriptome revealed a robust down-regulation of developmental PCD genes and an up-regulation of the genes involved in hypersensitive PCD triggered by nonhost-pathogen interactions. Accordingly, the BiP-overexpressing line displayed delayed leaf senescence under normal conditions and accelerated hypersensitive response triggered by Pseudomonas syringae pv tomato in soybean (Glycine max) and tobacco (Nicotiana tabacum), as monitored by measuring hallmarks of PCD in plants. The BiP-mediated delay of leaf senescence correlated with the attenuation of N-rich protein (NRP)-mediated cell death signaling and the inhibition of the senescence-associated activation of the unfolded protein response (UPR). By contrast, under biological activation of salicylic acid (SA) signaling and hypersensitive PCD, BiP overexpression further induced NRP-mediated cell death signaling and antagonistically inhibited the UPR. Thus, the SA-mediated induction of NRP cell death signaling occurs via a pathway distinct from UPR. Our data indicate that during the hypersensitive PCD, BiP positively regulates the NRP cell death signaling through a yet undefined mechanism that is activated by SA signaling and related to ER functioning. By contrast, BiP's negative regulation of leaf senescence may be linked to its capacity to attenuate the UPR activation and NRP cell death signaling. Therefore, BiP can function either as a negative or positive modulator of PCD events.
结合蛋白（BiP）已被证明参与先天免疫，并减轻内质网和渗透压应激诱导的细胞死亡。在这里，我们利用操纵 BiP 水平的转基因植物来评估 BiP 是否也控制发育和过敏性程序性细胞死亡（PCD）。在正常情况下，BiP 诱导的转录组显示出发育性 PCD 基因的强烈下调和非宿主-病原体相互作用触发的过敏性 PCD 相关基因的上调。因此，BiP 过表达系在正常条件下表现出延迟的叶片衰老，并且在大豆（Glycine max）和烟草（Nicotiana tabacum）中由丁香假单胞菌 pv 番茄触发的过敏性反应加速，如通过测量植物中 PCD 的标志来监测。BiP 介导的叶片衰老延迟与 N-丰富蛋白（NRP）介导的细胞死亡信号的衰减以及衰老相关的未折叠蛋白反应（UPR）的抑制相关。相比之下，在水杨酸（SA）信号和过敏性 PCD 的生物学激活下，BiP 过表达进一步诱导 NRP 介导的细胞死亡信号，并拮抗地抑制 UPR。因此，SA 介导的 NRP 细胞死亡信号的诱导通过与 UPR 不同的途径发生。我们的数据表明，在过敏性 PCD 期间，BiP 通过一种尚未定义的机制正向调节 NRP 细胞死亡信号，该机制通过 SA 信号和与 ER 功能相关的机制被激活。相比之下，BiP 对叶片衰老的负调节可能与其减弱 UPR 激活和 NRP 细胞死亡信号的能力有关。因此，BiP 可以作为 PCD 事件的负或正调节剂发挥作用。
