Staff Publications

Staff Publications

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    'Staff publications' is the digital repository of Wageningen University & Research

    'Staff publications' contains references to publications authored by Wageningen University staff from 1976 onward.

    Publications authored by the staff of the Research Institutes are available from 1995 onwards.

    Full text documents are added when available. The database is updated daily and currently holds about 240,000 items, of which 72,000 in open access.

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Record number 335018
Title A mysterious, pleiotropic growth defect caused by deletion of a glyoxal oxidase gene in Botrytis cinerea
Author(s) Kan, J.A.L. van; Stefanato, F.; Raats, E.M.
Source In: Book of Abstracts 7th European Conference on Fungal Genetics, Copenhagen, Denmark, 17-20 April 2004 - p. 168 - 168.
Department(s) Laboratory of Phytopathology
Publication type Abstract in scientific journal or proceedings
Publication year 2004
Abstract A Botrytis cinerea gene was cloned encoding a glyoxal oxidase homologue (BcGLYOX1). The gene product is presumably secreted and contains a chitin-binding domain homologous to plant lectins. BcGLYOX1 was anticipated to be required for production of oxalic acid and for virulence of this plant pathogenic fungus. Mutants constructed by gene replacement retained the ability to produce oxalic acid, indicating that BcGLYOX1 is not essential for oxalate production. Unexpectedly however, BcGLYOX1-deficient mutants lost the ability to germinate and grow on minimal media containing a range of carbon sources. The mutants were consequently non-pathogenic on a range of host tissues. The growth defect was fully restored by supplementing the medium with arginine at concentrations as low as 50 mM. Spontaneous suppressor mutants that regain the ability to grow on simple sugars in the absence of arginine were obtained at a frequency of about 10-6. introduction of the wild type gene into the mutant only partly restored the wild type growth phenotype. We conclude that the BcGLYOX1 mutation results in a severe defect in primary or secondary metabolism, which can be overcome by arginine supplementation. The mechanisms underlying the behaviour of the mutants, the relief of the phenotype by arginine, as well as the emergence of spontaneous suppressors remain elusive.
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