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Inhibition of signal transduction leading to appressorium formation in Magnaporthe grisea by glisoprenins

机译:抑制信号转导,导致Glisopthenrins在Magnaporthe Grisea中形成的植入膜

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From submerged cultures of the deuteromycete Gliocladium roseum, strain HA190-95, glisoprenins A, C, D and E were isolated as inhibitors of appressorium formation in Magnaporthe grisea. The compounds inhibited formation of infection structures on hydrophobic, stimulating surfaces. Glisoprenin E was ten times less active compared to the other glisoprenins. Formation of appressoria on nonstimulating surfaces, induced by the cAMP analogue 8-(4-chloro-phenylthio)-adenosine-3',5'-monophosphate or by 1,16-hexadecanediol, a plant wax component, was not affected by glisoprenins, indicating that at least two signal transduction pathways are involved in appressorium formation in M. grisea. Inhibition of appressorium development by glisoprenins on hydrophobic surface could be reversed in a competitive manner by 1,2-dioctanoylglycerol, a known activator of protein kinase C (PKC) but not by 1-oleoyl-2-acetylglycerol, the most effective inducer of PKC in mammalian cells.
机译:从氘霉素的浸没培养物中,菌株HA190-95,菌株HA190-95,Glisoprenα,C,D和E被隔离为Magnaporthe Grisea中抑制剂的抑制剂。该化合物抑制疏水性,刺激表面上的感染结构的形成。与其他Glisoprenins相比,Glisoprenin E的活性少了十倍。在非刺激表面上形成映像,由CAMP类似物8-(4-氯 - 苯硫基) - 吲哚-3',5'-单磷酸盐或1,16-十六烷二醇,植物蜡组分诱导,植物蜡组分不受Glisoprenins的影响,表明,在M.Grisea中涉及至少两个信号转导途径。通过Glisoprenins对疏水表面的抑制抑制疏水性表面可以通过1,2-二辛酰基甘油,一种已知的蛋白激酶C(PKC),但不是1-Oxyl-2-乙酰甘油,PKC最有效的诱导剂,以竞争的方式逆转在哺乳动物细胞中。

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