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Cloning of the pathogenicity-related gene <Emphasis Type="Italic">FPD1</Emphasis> in <Emphasis Type="Italic">Fusarium oxysporum</Emphasis> f. sp. <Emphasis Type="Italic">lycopersici</Emphasis>
Authors:Masato?Kawabe  Kohei?Mizutani  Takanobu?Yoshida  Tohru?Teraoka  Katsuyoshi?Yoneyama  Isamu?Yamaguchi  Email author" target="_blank">Tsutomu?ArieEmail author
Institution:(1) United Graduate School of Agricultural Science, Tokyo University of Agriculture and Technology (TUAT), Tokyo, Japan;(2) Laboratory of Plant Pathology, Faculty of Agriculture, Tokyo University of Agriculture and Technology (TUAT), 3-5-8 Saiwaicho, Fuchu, Tokyo, 183-8509, Japan;(3) Department of Biological Safety, National Institute for Agro-Enviromental Science (NIAES), Ibaraki, Japan;(4) Faculty of Agriculture, Meiji University, Kanagawa, Japan;(5) Enviromental Plant Research Group, RIKEN Plant Science Center, Kanagawa, Japan
Abstract:We selected a reduced-pathogenicity mutant of Fusarium oxysporum f. sp. lycopersici, a tomato wilt pathogen, from the transformants generated by restriction enzyme-mediated integration (REMI) transformation. The gene tagged with the plasmid in the mutant was predicted to encode a protein of 321 amino acids and was designated FPD1. Homology search showed its partial similarity to a chloride conductance regulatory protein of Xenopus, suggesting that FPD1 is a transmembrane protein. Although the function of FPD1 has not been identified, it does participate in the pathogenicity of F. oxysporum f. sp. lycopersici because FPD1-deficient mutants reproduced the reduced pathogenicity on tomato.The nucleotide sequence data reported are available in the DDBJ/EMBL/GenBank databases under the accession number AB110097
Keywords:Fusarium oxysporum  Pathogenicity  Tomato  REMI  ICln
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