Lorito M, Farkas V, Rebuffat S, Bodo B, Kubicek C P
Instituto di Patologia Vegetale, Università degli Studi di Napoli Federico II and Centro per lo Studio CNR delle Tecniche di Lotta Biologica, Naples, Italy.
J Bacteriol. 1996 Nov;178(21):6382-5. doi: 10.1128/jb.178.21.6382-6385.1996.
We have investigated the molecular basis for the reported synergism between peptaibols and cell wall hydrolytic enzymes in the antagonism of phytopathogenic fungi by Trichoderma harzianum. beta-Glucan synthase activity on isolated plasma membranes of Botrytis cinerea was inhibited in vitro by the peptaibols trichorzianin TA and TB, and this inhibition was reversed by the addition of phosphatidylcholine. beta-Glucan synthesis in vivo, assayed by the incorporation of [2-(3)H]glucose into cell wall material, was inhibited by the presence of peptaibols, and this inhibition was synergistic with exogenously added T. harzianum beta-1,3-glucanase. This synergism is therefore explained by an inhibition of the membrane-bound beta-1,3-glucan synthase of the host by the peptaibols, which inhibit the resynthesis of cell wall beta-glucans, sustain the disruptive action of beta-glucanases, and all together enhance the fungicidal activity. Therefore, we have identified cell wall turnover as a major target of mycoparasitic antagonism.
我们研究了哈茨木霉在拮抗植物病原真菌过程中,所报道的肽菌素与细胞壁水解酶之间协同作用的分子基础。在体外,肽菌素木霉毒素TA和TB抑制了灰葡萄孢菌分离质膜上的β-葡聚糖合酶活性,而添加磷脂酰胆碱可逆转这种抑制作用。通过将[2-(3)H]葡萄糖掺入细胞壁物质来测定的体内β-葡聚糖合成,受到肽菌素的抑制,并且这种抑制作用与外源添加的哈茨木霉β-1,3-葡聚糖酶具有协同性。因此,这种协同作用可以解释为肽菌素抑制了宿主膜结合的β-1,3-葡聚糖合酶,该酶抑制了细胞壁β-葡聚糖的重新合成,维持了β-葡聚糖酶的破坏作用,并共同增强了杀真菌活性。因此,我们已确定细胞壁周转是真菌寄生拮抗作用的主要靶点。