1988 Fiscal Year Final Research Report Summary
Genetic analysis of genes in mutants of graminicolous leaf-blight fungi
| Project/Area Number |
61560053
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
植物保護
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| Research Institution | Kyoto University |
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Principal Investigator |
TSUDA Mitsuya Faculty of Agriculture Associate Professor, 農学部, 助教授 (10026578)
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| Co-Investigator(Kenkyū-buntansha) |
TSUDA Mitsuya Faculty of Agriculture Associate Professor (10024423)
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| Project Period (FY) |
1986 – 1988
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| Keywords | Teleomorph / Ascospore / Mutation / Melanin / Cochliobolus hetrostrophus / Leaf-blight / Polyoxin / ネクトリア |
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| Research Abstract |
Crossing experiments with mutants genes, that reveal genetic information about plant pathogenic fungi are essential for elucidationg the nature of these parasites. In this project, I have confirmed the basis for ascospore analysis of graminicolous leaf-blight fungi by using teleomorph formation with mutant genes in vitro.
1. Anamorph-teleomorph connection in some plant pathogenic fungi and its application; Anamorph-teleomorph connection in some plant pathogenic fungi including graminicolous leaf-blight fungi were summarized. Ascocarp-ascospore production under controlled laboratory conditions have demonstrated and compared with conidium production. Ascospore dispersion of the causal agent of Nectria blight of Piper nigrum in the field was also confirmed.
2. Comparison of mutagenes in Cochliobolus heterostrophus mutagenesis; Lethal and mutagenic effects of four kinds of mutagenes (N-methyl-N-nitro-N-nitrosoguanidine(MNNG) ethyl methanesulfonate(EMS), UV light, -ray) on the fungus were studied. MNNG and EMS are almost equally effective in inducing the mutants. The maximum frequency of mutants among the suvaivors was at ca. 5 % survival in MNNG treatment and at 1.4 % survaival in EMS treatment.
3. Genetic analysis of genes in mutants of Cochliobolus heterostrophus; Five types of color mutants were obtained through chemical mutagenesis. The genetic deficient sites of the mutants were determined. The genetic deficient sites of mutants carring Albl,Scy,Brn, and Pgr were at the cyclization of pentaketide, conversion of scytalone, conversion of 1,3,8-THN, and oxidation of 1,8-DHN respectively, in the melanin biosynthesis. The results of crossing experiments indicated that lbl,Alb2 and Brn were closely linked, and that Scy and Pgr were same linkage group. Polyoxin resistant mutant carring Pol was also obtained. Pol was segregated indipendently from above mentioned loci.
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