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非典型 E2F 转录抑制因子 DEL1 通过控制激素水杨酸在植物生长和免疫的交汇点发挥作用。

Atypical E2F transcriptional repressor DEL1 acts at the intersection of plant growth and immunity by controlling the hormone salicylic acid.

机构信息

Department of Plant and Microbial Biology, University of California, Berkeley, CA 94720-3102, USA.

Department of Plant and Microbial Biology, University of California, Berkeley, CA 94720-3102, USA.

出版信息

Cell Host Microbe. 2014 Apr 9;15(4):506-13. doi: 10.1016/j.chom.2014.03.007.

Abstract

In plants, the activation of immunity is often inversely correlated with growth. Mechanisms that control plant growth in the context of pathogen challenge and immunity are unclear. Investigating Arabidopsis infection with the powdery mildew fungus, we find that the Arabidopsis atypical E2F DEL1, a transcriptional repressor known to promote cell proliferation, represses accumulation of the hormone salicylic acid (SA), an established regulator of plant immunity. DEL1-deficient plants are more resistant to pathogens and slightly smaller than wild-type. The resistance and size phenotypes of DEL1-deficient plants are due to the induction of SA and activation of immunity in the absence of pathogen challenge. Moreover, Enhanced Disease Susceptibility 5 (EDS5), a SA transporter required for elevated SA and immunity, is a direct repressed target of DEL1. Together, these findings indicate that DEL1 control of SA levels contributes to regulating the balance between growth and immunity in developing leaves.

摘要

在植物中,免疫的激活通常与生长呈负相关。在病原体挑战和免疫的背景下控制植物生长的机制尚不清楚。通过研究拟南芥感染白粉菌,我们发现拟南芥非典型 E2F DEL1,一种已知促进细胞增殖的转录抑制剂,抑制了植物免疫调节剂水杨酸(SA)的积累。DEL1 缺陷型植物对病原体的抗性更强,且比野生型略小。DEL1 缺陷型植物的抗性和大小表型是由于在没有病原体挑战的情况下诱导了 SA 和激活了免疫。此外,水杨酸转运蛋白增强疾病易感性 5(EDS5)是提高 SA 和免疫所必需的,是 DEL1 的直接受抑制靶标。这些发现表明,DEL1 控制 SA 水平有助于调节发育中的叶片中生长和免疫之间的平衡。

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