Departamento de Bioquímica, Facultad de Química, Universidad Nacional Autónoma de México, 04510 Mexico D.F., Mexico.
Planta. 2013 Jan;237(1):121-36. doi: 10.1007/s00425-012-1758-z. Epub 2012 Sep 19.
Sphingolipids play an important role in signal transduction pathways that regulate physiological functions and stress responses in eukaryotes. In plants, recent evidence suggests that their metabolic precursors, the long-chain bases (LCBs) act as bioactive molecules in the immune response. Interestingly, the virulence of two unrelated necrotrophic fungi, Fusarium verticillioides and Alternaria alternata, which are pathogens of maize and tomato plants, respectively, depends on the production of sphinganine-analog mycotoxins (SAMs). These metabolites inhibit de novo synthesis of sphingolipids in their hosts causing accumulation of LCBs, which are key regulators of programmed cell death. Therefore, to gain more insight into the role of sphingolipids in plant immunity against SAM-producing necrotrophic fungi, we disrupted sphingolipid metabolism in Nicotiana benthamiana through virus-induced gene silencing (VIGS) of the serine palmitoyltransfersase (SPT). This enzyme catalyzes the first reaction in LCB synthesis. VIGS of SPT profoundly affected N. benthamiana development as well as LCB composition of sphingolipids. While total levels of phytosphingosine decreased, sphinganine and sphingosine levels increased in SPT-silenced plants, compared with control plants. Plant immunity was also affected as silenced plants accumulated salicylic acid (SA), constitutively expressed the SA-inducible NbPR-1 gene and showed increased susceptibility to the necrotroph A. alternata f. sp. lycopersici. In contrast, expression of NbPR-2 and NbPR-3 genes was delayed in silenced plants upon fungal infection. Our results strongly suggest that LCBs modulate the SA-dependent responses and provide a working model of the potential role of SAMs from necrotrophic fungi to disrupt the plant host response to foster colonization.
鞘脂类在调节真核生物生理功能和应激反应的信号转导途径中发挥着重要作用。在植物中，最近的证据表明，其代谢前体——长链碱基（LCB）作为免疫反应中的生物活性分子发挥作用。有趣的是，两种不相关的坏死型真菌——分别为玉米和番茄病原菌的尖孢镰刀菌（Fusarium verticillioides）和链格孢菌（Alternaria alternata）的毒力依赖于麦角甾醇类似物真菌毒素（SAM）的产生。这些代谢物抑制宿主中鞘脂的从头合成，导致 LCB 的积累，而 LCB 是程序性细胞死亡的关键调节剂。因此，为了更深入地了解鞘脂在植物对产生 SAM 的坏死型真菌的免疫中的作用，我们通过病毒诱导的基因沉默（VIGS）丝氨酸棕榈酰转移酶（SPT）破坏了烟草原生质体中的鞘脂代谢。该酶催化 LCB 合成的第一步反应。SPT 的 VIGS 严重影响了烟草原生质体的发育以及鞘脂的 LCB 组成。与对照植物相比，沉默植物中植烷醇的总水平降低，而神经酰胺和鞘氨醇的水平增加。植物的免疫也受到影响，因为沉默植物积累水杨酸（SA），组成型表达 SA 诱导的 NbPR-1 基因，并对坏死型病原菌 A. alternata f. sp. lycopersici 的敏感性增加。相比之下，沉默植物在真菌感染时 NbPR-2 和 NbPR-3 基因的表达延迟。我们的结果强烈表明，LCB 调节 SA 依赖性反应，并为坏死型真菌的 SAM 破坏植物宿主对定殖的反应提供了一个作用模型。
