Abstract：
In plant biology Fusicoccin (FC) is one of the most studied fungal metabolites to date. Since the structural identification in 1964, much has been learned about its effects on the physiology of plants, about the interference with the action of plant hormones, the molecular nature of the plant receptor(s) for FC and the biosynthetic pathway for FC in the fungus. The finding that the plasma membrane H+-ATPase in combination with 14-3-3 proteins acts as high-affinity receptor for FC was a breakthrough in the field. Ever since, the binding of FC to the ATPase|14-3-3 receptor has taken center stage in explaining all FC induced physiological effects. However, a more critical review shows that this is not at all evident for a number of FC induced effects. Examples of this are: the inhibition of outward rectifying K+-channels in guard cells, the phosphorylation/activation of PEP-carboxylase and malate accumulation, the antagonism with ABA induced production of H2O2 / NO and the effect on ethylene production. In addition, recently two other physiological processes were shown to be targeted by FC, viz. the activation of TORC1 and the interference of FC with the immune response to fungal elicitors. In this review, the notion will be challenged that all FC affected processes start with the binding to and activation of the PM-ATPase and the question is raised whether may be other proteins with a key role in the respective processes are directly targeted by FC. A second unresolved question is whether FC may be another example of a fungal molecule turning out to be a \'copy\' of an as yet unknown plant molecule; in analogy to the fungal product and plant hormone gibberellic acid. A relevant question in this respect is whether it is a coincidence that proteins that act in a coordinated fashion during stomatal opening (the ATPases and K+-channels) are targeted by FC? Or are the sites where FC binds in the plant, conserved during evolution because they serve a physiological role, namely the accommodation of a plant produced molecule? In view of the evidence, albeit not conclusive, that plants indeed produce \'FC-like ligands\', it is worthwhile to make a renewed attempt with current day improved technology to answer this question and may be upgrade FC or structural analogue(s) to a new level, the level of plant hormone.
摘要：
在植物生物学中，Fusicocin（FC）是迄今为止研究最多的真菌代谢产物之一。自1964年的结构鉴定以来，人们对其对植物生理的影响有了很多了解，关于植物激素作用的干扰，FC的植物受体的分子性质和真菌中FC的生物合成途径。发现质膜H-ATPase与14-3-3蛋白组合充当FC的高亲和力受体是该领域的突破。从那以后，FC与ATPase|14-3-3受体的结合已成为解释所有FC诱导的生理作用的中心阶段。然而,更严格的审查表明，这一点对于许多FC诱导的影响并不明显。这方面的例子是：保护细胞中向外整流K+通道的抑制，PEP-羧化酶的磷酸化/激活和苹果酸积累，与ABA的拮抗作用诱导了H2O2/NO的产生以及对乙烯产生的影响。此外,最近，另外两个生理过程被证明是FC的目标，viz.TORC1的激活和FC对真菌诱导子免疫应答的干扰。在这次审查中,所有受FC影响的过程都是从PM-ATPase的结合和激活开始的概念将受到挑战，并且提出了一个问题，即FC是否直接针对在各个过程中起关键作用的其他蛋白质。第二个未解决的问题是，FC是否可能是真菌分子的另一个例子，结果是未知的植物分子的“拷贝”；类似于真菌产品和植物激素赤霉酸。在这方面的一个相关问题是，在气孔开放过程中以协调方式起作用的蛋白质（ATPases和K通道）被FC靶向是否是巧合？还是FC在植物中结合的位点，在进化过程中保守，因为它们具有生理作用，即植物产生的分子的适应？鉴于证据，尽管没有定论，植物确实产生了“FC样配体”，这是值得作出新的尝试与当前的改进技术来回答这个问题，并可能升级FC或结构模拟（S）到一个新的水平，植物激素的水平。
