Zhang S, Klessig D F
Waksman Institute and Department of Molecular Biology and Biochemistry, Rutgers University, 190 Frelinghuysen Road, Piscataway, NJ 08854-8020, USA.
Proc Natl Acad Sci U S A. 1998 Jun 23;95(13):7433-8. doi: 10.1073/pnas.95.13.7433.
Salicylic acid-induced protein kinase (SIPK) and wounding-induced protein kinase (WIPK), two distinct members of the mitogen-activated protein (MAP) kinase family, are activated in tobacco resisting infection by tobacco mosaic virus (TMV). WIPK activation by TMV depends on the disease-resistance gene N because infection of susceptible tobacco not carrying the N gene failed to activate WIPK. Activation of WIPK required not only posttranslational phosphorylation but also a preceding rise in its mRNA and de novo synthesis of WIPK protein. The induction by TMV of WIPK mRNA and protein also occurred systemically. Its activation at the mRNA, protein, and enzyme levels was independent of salicylic acid. The regulation of WIPK at multiple levels by an N gene-mediated signal(s) suggests that this MAP kinase may be an important component upstream of salicylic acid in the signal-transduction pathway(s) leading to local and systemic resistance to TMV.
水杨酸诱导蛋白激酶(SIPK)和创伤诱导蛋白激酶(WIPK)是丝裂原活化蛋白(MAP)激酶家族的两个不同成员,在烟草抵抗烟草花叶病毒(TMV)感染的过程中被激活。TMV对WIPK的激活依赖于抗病基因N,因为未携带N基因的感病烟草在感染后无法激活WIPK。WIPK的激活不仅需要翻译后磷酸化,还需要其mRNA的先上升以及WIPK蛋白的从头合成。TMV对WIPK mRNA和蛋白的诱导也会系统性地发生。其在mRNA、蛋白和酶水平的激活与水杨酸无关。由N基因介导的信号在多个水平对WIPK的调控表明,这种MAP激酶可能是水杨酸上游信号转导途径中导致对TMV产生局部和系统抗性的重要组成部分。