Kashiwa Takeshi, Suzuki Tatsuya, Sato Akira, Akai Kotaro, Teraoka Tohru, Komatsu Ken, Arie Tsutomu
Graduate School of Agriculture, Tokyo University of Agriculture and Technology (TUAT), Fuchu, Tokyo 183-8509, Japan.
Chiba Prefectural Agriculture and Forestry Research Center, 808 Daizenno-cho, Midori-ku, Chiba 266-0006, Japan.
FEMS Microbiol Lett. 2016 Jul;363(14). doi: 10.1093/femsle/fnw132. Epub 2016 May 17.
Emergence of races in Fusarium oxysporum f. sp. lycopersici (Fol) is caused by loss or mutation of at least one avirulence (AVR) gene. The product of AVR1 is a small protein (Avr1) secreted by Fol in tomato xylem sap during infection. This protein triggers Fol race 1 specific resistance (I) in tomato, indicating that AVR1 is an AVR gene. Deletion of AVR1 in race 1 resulted in the emergence of race 2, and an additional mutation in AVR2 generated race 3. Previously, we reported a new biotype of race 3, KoChi-1, in which AVR1 was truncated by a transposon Hormin, which suggested a new route to evolution of races in Fol However, to date no race 2 isolate carrying Hormin-truncated AVR1 has been reported. In this report, we describe such isolates, represented by Chiba-5, in which Hormin insertion occurred in AVR1 at a position different from that in KoChi-1. AVR1 truncation in both isolates resulted in production of defective Avr1 proteins. Chiba-5 and KoChi-1 belong to different phylogenetic clades, A1 and A2, respectively, suggesting that insertion of Hormin in AVR1 in Chiba-5 and KoChi-1 occurred as independent evolutionary events.
尖孢镰刀菌番茄专化型(Fusarium oxysporum f. sp. lycopersici,Fol)中不同生理小种的出现是由至少一个无毒(AVR)基因的缺失或突变引起的。AVR1的产物是一种小蛋白(Avr1),在感染期间由Fol分泌到番茄木质部汁液中。这种蛋白在番茄中触发Fol生理小种1特异性抗性(I),表明AVR1是一个AVR基因。生理小种1中AVR1的缺失导致了生理小种2的出现,而AVR2中的另一个突变产生了生理小种3。此前,我们报道了生理小种3的一种新生物型KoChi-1,其中AVR1被转座子Hormin截断,这提示了Fol中生理小种进化的一条新途径。然而,迄今为止,尚未报道携带Hormin截断的AVR1的生理小种2分离株。在本报告中,我们描述了以千叶-5(Chiba-5)为代表的此类分离株,其中Hormin插入AVR1的位置与KoChi-1中的不同。两个分离株中AVR1的截断均导致产生有缺陷的Avr1蛋白。千叶-5和KoChi-1分别属于不同的系统发育分支A1和A2,这表明千叶-5和KoChi-1中Hormin插入AVR1是独立的进化事件。