Salzer P, Hübner B, Sirrenberg A, Hager A
Botanisches Institut der Universität Tübingen, Germany.
Plant Physiol. 1997 Jul;114(3):957-68. doi: 10.1104/pp.114.3.957.
Two chitinases (EC 3.2.1.14) and two beta-1,3-glucanases (EC 3.2.1.39) were purified from the culture medium of spruce (Picea abines [L.] Karst.) cells to study their role in modifying elicitors, cell walls, growth, and hyphal morphology of ectomycorrhizal fungi. The 36-kD class I chitinase (isoelectric point [pl] 8.0) and the 28-kD chitinase (pl 8.7) decreased the activity of elicitor preparations from Hebeloma crustuliniforme (Bull. ex Fries.) Quél., Amanita muscaria (L.) Pers., and Suillus variegatus (Sw.: Fr.) O.K., as demonstrated by using the elicitor-induced extracellular alkalinization in spruce cells as a test system. In addition, chitinases released monomeric products from the walls of these ectomycorrhizal fungi. The beta-1,3-glucanases (35 kD, pl 3.7 and 3.9), in contrast, had little influence on the activity of the fungal elicitors and released only from walls of A. muscaria some polymeric products. Furthermore, chitinases alone and in combination with beta-1,3-glucanases had no effect on the growth and morphology of the hyphae. Thus, it is suggested that apoplastic chitinases in the root cortex destroy elicitors from the ectomycorrhizal fungi without damaging the fungus. By this mechanism the host plant could attenuate the elicitor signal and adjust its own defense reactions to a level allowing symbiotic interaction.
从云杉(Picea abines [L.] Karst.)细胞培养基中纯化出两种几丁质酶(EC 3.2.1.14)和两种β-1,3-葡聚糖酶(EC 3.2.1.39),以研究它们在修饰外生菌根真菌的激发子、细胞壁、生长及菌丝形态方面的作用。通过使用云杉细胞中激发子诱导的细胞外碱化作为测试系统,证明36-kD的I类几丁质酶(等电点[pl] 8.0)和28-kD的几丁质酶(pl 8.7)降低了来自卷边靴耳(Hebeloma crustuliniforme (Bull. ex Fries.) Quél.)、毒蝇鹅膏(Amanita muscaria (L.) Pers.)和杂色乳牛肝菌(Suillus variegatus (Sw.: Fr.) O.K.)的激发子制剂的活性。此外,几丁质酶从这些外生菌根真菌的细胞壁释放出单体产物。相比之下,β-1,3-葡聚糖酶(35 kD,pl 3.7和3.9)对真菌激发子的活性影响很小,并且仅从毒蝇鹅膏的细胞壁释放出一些聚合产物。此外,单独的几丁质酶以及与β-1,3-葡聚糖酶组合使用时,对菌丝的生长和形态没有影响。因此,有人提出根皮层中的质外体几丁质酶可破坏外生菌根真菌的激发子而不损害真菌。通过这种机制,宿主植物可以减弱激发子信号,并将自身的防御反应调节到允许共生相互作用的水平。