Beffa R S, Neuhaus J M, Meins F
Friedrich Miescher Institute, Basel, Switzerland.
Proc Natl Acad Sci U S A. 1993 Oct 1;90(19):8792-6. doi: 10.1073/pnas.90.19.8792.
Plant class I glucan endo-1,3-beta-glucosidases (beta-1,3-glucanase; 1,3-beta-D-glucan glucanohydrolase, EC 3.2.1.39) have been implicated in development and defense against pathogen attack. Nevertheless, beta-1,3-glucanase deficiencies generated by antisense transformation of Nicotiana sylvestris and tobacco have little biological effect. We report here that another beta-1,3-glucanase activity is induced in these deficient mutants after infection with necrotizing viruses. Induction of class I beta-1,3-glucanase was markedly inhibited in leaves of N. sylvestris and tobacco antisense transformants infected with tobacco necrosis virus and tobacco mosaic virus, respectively. A serologically distinct beta-1,3-glucanase activity was present in the infected antisense transformants but was absent in both healthy and infected control plants and in antisense transformants treated with the stress hormone ethylene. Immunoblot analyses, localization studies, and measurements of antibody specificity indicate that this compensatory beta-1,3-glucanase activity is an intracellular enzyme different from known tobacco beta-1,3-glucanases. Therefore, plants can compensate for a deficiency in enzyme activity by producing a functionally equivalent replacement--i.e., "ersatz"--protein or proteins. The fact that compensation for beta-1,3-glucanase activity occurs in response to infection argues strongly for an important role of these enzymes in pathogenesis.
植物I类葡聚糖内切-1,3-β-葡糖苷酶（β-1,3-葡聚糖酶；1,3-β-D-葡聚糖葡聚糖水解酶，EC 3.2.1.39）与植物发育以及抵御病原体侵袭有关。然而，通过对野生烟草和烟草进行反义转化产生的β-1,3-葡聚糖酶缺陷几乎没有生物学效应。我们在此报告，在这些缺陷突变体被坏死病毒感染后，会诱导产生另一种β-1,3-葡聚糖酶活性。分别在感染烟草坏死病毒和烟草花叶病毒的野生烟草和烟草反义转化体的叶片中，I类β-1,3-葡聚糖酶的诱导受到显著抑制。在受感染的反义转化体中存在一种血清学上不同的β-1,3-葡聚糖酶活性，但在健康和受感染的对照植物以及用应激激素乙烯处理的反义转化体中均不存在。免疫印迹分析、定位研究以及抗体特异性测量表明，这种补偿性β-1,3-葡聚糖酶活性是一种细胞内酶，与已知的烟草β-1,3-葡聚糖酶不同。因此，植物可以通过产生功能等效的替代蛋白（即“替代”蛋白）来弥补酶活性缺陷。β-1,3-葡聚糖酶活性补偿是对感染作出的反应，这一事实有力地证明了这些酶在发病机制中起重要作用。
