Cloned (Comment) | Organism |
---|---|
gene gene Ss-oah1, DNA and amino acid sequence determination and analysis, PCR-based genome walking | Sclerotinia sclerotiorum |
Protein Variants | Comment | Organism |
---|---|---|
additional information | generation of gene deletion DELTAss-oah1 mutants | Sclerotinia sclerotiorum |
Natural Substrates | Organism | Comment (Nat. Sub.) | Natural Products | Comment (Nat. Pro.) | Rev. | Reac. |
---|---|---|---|---|---|---|
oxaloacetate + H2O | Sclerotinia sclerotiorum | - |
oxalate + acetate | - |
? | |
oxaloacetate + H2O | Sclerotinia sclerotiorum 1980 | - |
oxalate + acetate | - |
? |
Organism | UniProt | Comment | Textmining |
---|---|---|---|
Sclerotinia sclerotiorum | A7ESB3 | gene Ss-oah1 | - |
Sclerotinia sclerotiorum 1980 | A7ESB3 | gene Ss-oah1 | - |
Source Tissue | Comment | Organism | Textmining |
---|---|---|---|
leaf | - |
Sclerotinia sclerotiorum | - |
Substrates | Comment Substrates | Organism | Products | Comment (Products) | Rev. | Reac. |
---|---|---|---|---|---|---|
oxaloacetate + H2O | - |
Sclerotinia sclerotiorum | oxalate + acetate | - |
? | |
oxaloacetate + H2O | - |
Sclerotinia sclerotiorum 1980 | oxalate + acetate | - |
? |
Synonyms | Comment | Organism |
---|---|---|
OAH | - |
Sclerotinia sclerotiorum |
General Information | Comment | Organism |
---|---|---|
malfunction | gene deletion DELTAss-oah1 mutants do not accumulate oxalate in culture or during plant infection. The defect in oxalate accumulation is fully restored on reintroduction of the wild-type Ss-oah1gene. The DELTAss-oah1 mutants are deficient in compound appressorium and sclerotium development and exhibit a severe radial growth defect on medium buffered at neutral pH. On a variety of plant hosts, the DELTAss-oah1 mutants establish very restricted lesions in which the infectious hyphae gradually lose viability. Cytological comparisons of wild-type and DELTAss-oah1 infections reveal low and no oxalate accumulation, respectively, in subcuticular hyphae. Both wild-type and mutant hyphae exhibit a transient association with viable host epidermal cells at the infection front. DELTAss-oah1 mutants exhibit significantly attenuated virulence, e.g. in infected soybean leaves. Lesions generated by the GFP-labelled DELTAss-oah1 mutants expand slowly and are delimited within 3 days | Sclerotinia sclerotiorum |
physiological function | oxalate biogenesis in Sclerotinia. sclerotiorum appears to rely exclusively on oxaloacteate hydrolase-mediated C-C cleavage of oxaloacetate. During pathogenesis, oxalic acid accumulation is critical to the broad host range necrotrophic pathogenicity | Sclerotinia sclerotiorum |