Analysis of the Mechanisms for Soilborne Plant Disease Development using REMI-Mutants of Fusarium oxysporum

利用尖孢镰刀菌 REMI 突变体分析土传植物病害发展机制

基本信息

批准号：
12660051
负责人：
ARIE Tsutomu
金额：
$ 2.18万
依托单位：
Tokyo University of Agriculture and Technology, Faculty of Agriculture
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2000
资助国家：
日本
起止时间：
2000 至 2002
项目状态：
已结题

项目摘要

About 20 pathogenicity mutants of Fusarium oxysporum ff. sp. conglutinans (cabbage yellows pathogen ; FOC) and lycopersici (tomato wilt pathogen ; FOL) were selected from about 2500 transformants generated by restriction enzyme-mediated integration (REMI) mutagenesis.REMI10, a pathogenicity-deficient mutant of FOC, was proved that a copy of pCNS43 was inserted into the genome. The gene disrupted by the insertion of pCSN43 was rescued and the gene seemed to encode an aspartic proteinase. We designated the gene fap1. fapl disruptants of FOC carried pathogenicity to cabbage equilibrant with FOC, showed that FAP1 is not responsible to FOC for pathogenicity. Pretreatment of cabbage root with REMI10 reduced the disease incidence of yellows caused by FOC. This suggested that REMI 10 carried biocontrol activity. Behavior of green fluorescence protein (GFP)-expressing REMI10 (EGFP-REMI10) was observed under fluorescence microscope and we could see that EGFP-REMI10 penetrate into cabbage root through cuticle slower than FOC and EGFP-REMI10 did not go through the endodermis to the xylem even 14 days after inoculation.r-120, a reduced pathogenicity mutant of FOL, was also proved that a copy of pCNS43 was inserted into the genome. The gene tagged in the mutant with pCSN43 was predicted to encode a protein of 321 amino acids and designated foir1, Homology search showed its partial similarity to a chloride conductance regulatory protein of Xenopus laevis, suggesting that FOIR1 is a transmembrane protein. Although the role of FOIR1 has never been identified, it may participate to the pathogenicity in FOL, because FOIR1 deficient mutants of FOL reproduced reduced pathogenicity on tomato.

大约20个致病性突变体的氧气孢子虫FF。 sp。 Conglutinans（卷心菜对病原体; foc）和lycopersici（番茄枯萎病原体； for）从约2500个由限制酶介导的整合（REMI）诱变产生的大约2500个转化子中，证明了一种病原性的焦点，是一种病原体性突变体，证明了pcns43 copery centns43 segore copery copery copery copery copery cente negorome segore ins cen negore ins negore ins ceneme ins egorome。救出了被PCSN43插入的基因被挽救，该基因似乎编码了天冬氨酸蛋白酶。我们指定了基因FAP1。 FAPL携带的致病性对卷心菜与foc的致病性与焦点平衡，表明FAP1不承担致病性的责任。用REMI10进行卷心菜根的预处理可降低由焦点引起的黄色疾病的发生率。这表明REMI 10带有生物防治活性。 Behavior of green fluorescence protein (GFP)-expressing REMI10 (EGFP-REMI10) was observed under fluorescence microscope and we could see that EGFP-REMI10 penetrate into cabbage root through cuticle slower than FOC and EGFP-REMI10 did not go through the endodermis to the xylem even 14 days after inoculation.r-120, a reduced pathogenicity mutant of FOL, was also proved将PCNS43的副本插入了基因组中。预计用PCSN43在突变体中标记的基因被预测编码321个氨基酸的蛋白质并指定为FOIR1，同源性搜索显示其与Xenopus laevis的氯化物调节蛋白的部分相似性，表明FOIR1是foir1是一种跨膜蛋白。尽管从未鉴定出FOIR1的作用，但它可能参与FOL的致病性，因为FOIR1 FOL的缺乏突变体在番茄上降低了致病性。