Devarenne Timothy P, Ekengren Sophia K, Pedley Kerry F, Martin Gregory B
Boyce Thompson Institute for Plant Research, Cornell University, Ithaca, NY 14853-1801, USA.
EMBO J. 2006 Jan 11;25(1):255-65. doi: 10.1038/sj.emboj.7600910. Epub 2005 Dec 15.
Bacterial speck disease in tomato is caused by Pseudomonas syringae pv. tomato. Resistance to this disease is conferred by the host Pto kinase, which recognizes P. s. pv. tomato strains that express the effector AvrPto. We report here that an AvrPto-dependent Pto-interacting protein 3 (Adi3) is a member of the AGC family of protein kinases. In mammals, AGC kinases are regulated by 3-phosphoinositide-dependent protein kinase-1 (Pdk1). We characterized tomato Pdk1 and showed that Pdk1 and Pto phosphorylate Adi3. Gene silencing of Adi3 in tomato causes MAPKKKalpha-dependent formation of necrotic lesions. Use of a chemical inhibitor of Pdk1, OSU-03012, also implicates Pdk1 and Adi3 in plant cell death regulation. Adi3 thus appears to function analogously to the mammalian AGC kinase protein kinase B/Akt by negatively regulating cell death via Pdk1 phosphorylation. We speculate that the negative regulatory function of Adi3 might be subverted by interaction with Pto/AvrPto, leading to host cell death that is associated with pathogen attack.
番茄细菌性斑点病由丁香假单胞菌番茄致病变种(Pseudomonas syringae pv. tomato)引起。宿主的Pto激酶赋予了对该病的抗性,该激酶可识别表达效应子AvrPto的丁香假单胞菌番茄致病变种菌株。我们在此报告,一种依赖AvrPto的Pto相互作用蛋白3(Adi3)是AGC蛋白激酶家族的成员。在哺乳动物中,AGC激酶受3-磷酸肌醇依赖性蛋白激酶-1(Pdk1)调控。我们对番茄Pdk1进行了表征,结果表明Pdk1和Pto可使Adi3磷酸化。番茄中Adi3的基因沉默会导致依赖MAPKKKalpha的坏死斑形成。使用Pdk1的化学抑制剂OSU-03012也表明Pdk1和Adi3参与植物细胞死亡调控。因此,Adi3似乎通过Pdk1磷酸化负调控细胞死亡,其功能类似于哺乳动物的AGC激酶蛋白激酶B/Akt。我们推测,Adi3的负调控功能可能会因与Pto/AvrPto相互作用而被颠覆,从而导致与病原体攻击相关的宿主细胞死亡。