a genetic mechanism for emergence of races in fusarium oxysporum f. sp. lycopersici inactivation of avirulence gene avr1 by transposon insertion出现在尖孢镰刀菌的遗传机制f . sp.黄瓜无毒性基因的失活avr1转座子插入.pdfVIP

A Genetic Mechanism for Emergence of Races in Fusarium oxysporum f. sp. lycopersici: Inactivation of Avirulence Gene AVR1 by Transposon Insertion 1 1 2 1,2 1 Keigo Inami , Chizu Yoshioka-Akiyama , Yasuaki Morita , Mutsuko Yamasaki , Tohru Teraoka , Tsutomu Arie1* 1 Graduate School of Agriculture, Tokyo University of Agriculture and Technology (TUAT), Fuchu, Japan, 2 Kochi Agricultural Research Center, Nangoku, Japan Abstract Compatible/incompatible interactions between the tomato wilt fungus Fusarium oxysporum f. sp. lycopersici (FOL) and tomato Solanum lycopersicum are controlled by three avirulence genes (AVR1–3) in FOL and the corresponding resistance genes (I–I3) in tomato. The three known races (1, 2 and 3) of FOL carry AVR genes in different combinations. The current model to explain the proposed order of mutations in AVR genes is: i) FOL race 2 emerged from race 1 by losing the AVR1 and thus avoiding host resistance mediated by I (the resistance gene corresponding to AVR1), and ii) race 3 emerged when race 2 sustained a point mutation in AVR2, allowing it to evade I2-mediated resistance of the host. Here, an alternative mechanism of mutation of AVR genes was determined by analyses of a race 3 isolate, KoChi-1, that we recovered from a Japanese tomato field in 2008. Although KoChi-1 is race 3, it has an AVR1 gene that is truncated by the transposon Hormin, which belongs to the hAT family. This provides evidence that mobile genetic elements may be one of the driving forces underlying race evolution. KoChi-1 transformants carrying a wild type AVR1 gene from race 1 lost pathogenicity to cultivars carrying I, showing that th