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柠檬幼苗对链格孢菌过敏反应中肌醇三磷酸的产生涉及活性蛋白酪氨酸激酶而非G蛋白。

IP3 production in the hypersensitive response of lemon seedlings against Alternaria alternata involves active protein tyrosine kinases but not a G-protein.

作者信息

Ortega Ximena, Velásquez Juan Carlos, Pérez Luz M

机构信息

Laboratorio de Bioquímica, Facultad de Ciencias de la Salud, Universidad Andrés Bello, Santiago, Chile.

出版信息

Biol Res. 2005;38(1):89-99. doi: 10.4067/s0716-97602005000100011.

DOI:10.4067/s0716-97602005000100011
PMID:15977414
Abstract

IP3 increase and de novo synthesis of scoparone are produced in the hypersensitive response (HR) of lemon seedlings against the fungus Alternaria alternata. To elucidate whether a G-protein and/or a protein tyrosine kinase (PTK) are involved in signal transduction leading to the production of such a defensive response, we studied the HR in this plant system after treatment with G-protein activators alone and PTK inhibitors in the presence of fungal conidia. No changes in the level of IP3 were detected in response to the treatment with the G-protein activators cholera toxin or mastoparan, although the HR was observed in response to these compounds as determined by the scoparone synthesis. On the contrary, the PTK inhibitors lavendustin A and 2,5-dihidroxy methyl cinnamate (DHMC) not only prevented the IP3 changes observed in response to the fungal inoculation of lemon seedlings but also blocked the development of the HR. These results suggest that the IP3 changes observed in response to A. alternata require a PTK activity and are the result of a G-protein independent Phospholipase C activity, even though the activation of a G-protein can also lead to the development of a HR. Therefore, it appears that more than one signaling pathway may be activated for the development of HR in lemon seedlings: one involving a G-protein and the other involving a PTK-dependent PLC.

摘要

柠檬幼苗对真菌链格孢的过敏反应(HR)中会产生肌醇三磷酸(IP3)增加和滨蒿内酯的从头合成。为了阐明G蛋白和/或蛋白酪氨酸激酶(PTK)是否参与导致这种防御反应产生的信号转导,我们在真菌分生孢子存在的情况下,单独用G蛋白激活剂和PTK抑制剂处理该植物系统后,研究了其中的过敏反应。尽管通过滨蒿内酯合成确定对这些化合物有过敏反应,但用G蛋白激活剂霍乱毒素或 Mastoparan 处理后,未检测到IP3水平的变化。相反,PTK抑制剂薰衣草霉素A和2,5 - 二羟基甲基肉桂酸酯(DHMC)不仅阻止了柠檬幼苗接种真菌后观察到的IP3变化,还阻断了过敏反应的发展。这些结果表明,对链格孢反应中观察到的IP3变化需要PTK活性,并且是G蛋白非依赖性磷脂酶C活性的结果,尽管G蛋白的激活也可导致过敏反应的发展。因此,似乎柠檬幼苗过敏反应的发展可能激活了不止一条信号通路:一条涉及G蛋白,另一条涉及PTK依赖性磷脂酶C。

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