Wulff B B H, Chakrabarti A, Jones D A
Institut de Biologie Moléculaire des Plantes (IBMP-CNRS), 12 rue du Général Zimmer, 67084 Strasbourg, France.
Mol Plant Microbe Interact. 2009 Oct;22(10):1191-202. doi: 10.1094/MPMI-22-10-1191.
The interactions between plants and many biotrophic or hemibiotrophic pathogens are controlled by receptor proteins in the host and effector proteins delivered by the pathogen. Pathogen effectors facilitate pathogen growth through the suppression of host defenses and the manipulation of host metabolism, but recognition of a pathogen-effector protein by a host receptor enables the host to activate a suite of defense mechanisms that limit pathogen growth. In the tomato (Lycopersicon esculentum syn. Solanum lycopersicum)-Cladosporium fulvum (leaf mold fungus syn. Passalora fulva) pathosystem, the host receptors are plasma membrane-anchored, leucine-rich repeat, receptor-like proteins encoded by an array of Cf genes conferring resistance to C. fulvum. The pathogen effectors are mostly small, secreted, cysteine-rich, but otherwise largely dissimilar, extracellular proteins encoded by an array of avirulence (Avr) genes, so called because of their ability to trigger resistance and limit pathogen growth when the corresponding Cf gene is present in tomato. A number of Cf and Avr genes have been isolated, and details of the complex molecular interplay between tomato Cf proteins and C. fulvum effector proteins are beginning to emerge. Each effector appears to have a different role; probably most bind or modify different host proteins, but at least one has a passive role masking the pathogen. It is, therefore, not surprising that each effector is probably detected in a distinct and specific manner, some by direct binding, others as complexes with host proteins, and others via their modification of host proteins. The two papers accompanying this review contribute further to our understanding of the molecular specificity underlying effector perception by Cf proteins. This review, therefore, focuses on our current understanding of recognitional specificity in the tomato-C. fulvum pathosystem and highlights some of the critical questions that remain to be addressed. It also addresses the evolutionary causes and consequences of this specificity.
植物与许多活体营养型或半活体营养型病原体之间的相互作用由宿主中的受体蛋白和病原体传递的效应蛋白所控制。病原体效应蛋白通过抑制宿主防御和操纵宿主代谢来促进病原体生长，但是宿主受体对病原体效应蛋白的识别能使宿主激活一系列限制病原体生长的防御机制。在番茄（Lycopersicon esculentum syn. Solanum lycopersicum）-番茄叶霉病菌（Cladosporium fulvum syn. Passalora fulva）互作体系中，宿主受体是由一系列Cf基因编码的、锚定在质膜上的富含亮氨酸重复序列的类受体蛋白，这些基因赋予番茄对叶霉病菌的抗性。病原体效应蛋白大多是由一系列无毒（Avr）基因编码的、小的、分泌型的、富含半胱氨酸但在其他方面差异很大的细胞外蛋白，之所以这样称呼是因为当相应的Cf基因存在于番茄中时，它们能够引发抗性并限制病原体生长。多个Cf和Avr基因已被分离出来，番茄Cf蛋白与叶霉病菌效应蛋白之间复杂的分子相互作用细节也开始显现。每个效应蛋白似乎都有不同的作用；可能大多数效应蛋白结合或修饰不同的宿主蛋白，但至少有一个起被动作用，即掩盖病原体。因此，每种效应蛋白可能以独特而特异的方式被检测到也就不足为奇了，有些是通过直接结合，有些是作为与宿主蛋白的复合物，还有些是通过它们对宿主蛋白的修饰。随本综述一同发表的两篇论文进一步增进了我们对Cf蛋白识别效应蛋白背后分子特异性的理解。因此，本综述聚焦于我们目前对番茄-叶霉病菌互作体系中识别特异性的理解，并突出了一些有待解决的关键问题，并探讨了这种特异性的进化原因和结果。
