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PMID:28132080
Citation |
'Islam, KT, Bond, JP and Fakhoury, AM (2017) FvSNF1, the sucrose non-fermenting protein kinase gene of Fusarium virguliforme, is required for cell-wall-degrading enzymes expression and sudden death syndrome development in soybean. Curr. Genet. ' |
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Abstract |
Fusarium virguliforme is a soil-borne pathogenic fungus that causes sudden death syndrome (SDS) in soybean. Its pathogenicity is believed to require the activity of cell-wall-degrading enzymes (CWDEs). The sucrose non-fermenting protein kinase 1 gene (SNF1) is a key component of the glucose de-repression pathway in yeast, and a regulator of gene expression for CWDEs in some plant pathogenic fungi. To elucidate the functional role of the SNF1 homolog in F. virguliforme, FvSNF1 was disrupted using a split-marker strategy. Disruption of FvSNF1 in F. virguliforme abolishes galactose utilization and causes poor growth on xylose, arabinose and sucrose. However, the resulting Fvsnf1 mutant grew similar to wild-type and ectopic transformants on glucose, fructose, maltose, or pectin as the main source of carbon. The Fvsnf1 mutant displayed no expression of the gene-encoding galactose oxidase (GAO), a secretory enzyme that catalyzes oxidation of D-galactose. It also exhibited a significant reduction in the expression of several CWDE-coding genes in contrast to the wild-type strain. Greenhouse pathogenicity assays revealed that the Fvsnf1 mutant was severely impaired in its ability to cause SDS on challenged soybean plants. Microscopy and microtome studies on infected roots showed that the Fvsnf1 mutant was defective in colonizing vascular tissue of infected plants. Cross and longitudinal sections of infected roots stained with fluorescein-labeled wheat germ agglutinin and Congo red showed that the Fvsnf1 mutant failed to colonize the xylem vessels and phloem tissue at later stages of infection. Quantification of the fungal biomass in inoculated roots further confirmed a reduced colonization of roots by the Fvsnf1 mutant when compared to the wild type. These findings suggest that FvSNF1 regulates the expression of CWDEs in F. virguliforme, thus affecting the virulence of the fungus on soybean. |
Links |
PubMed Online version:10.1007/s00294-017-0676-9 |
Keywords |
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Significance
Annotations
Gene product | Qualifier | GO Term | Evidence Code | with/from | Aspect | Extension | Notes | Status |
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GO:0009405: pathogenesis |
ECO:0000314: |
P |
Figure 7B, fungus expressing mutant form of gene is not able to induce pathogenesis in host while fungus expressed in wild type gene is. strains tested were Mont - 1 and (Delta)SF18 FvSNF1 protien kinase gene of Fusarium virguliforme uniprot refers to it as Fusarium solani f. sp. glycines |
complete | ||||
GO:0044122: development of symbiont in host vascular tissue |
ECO:0000315: |
P |
Figure 8A,8B,and 8C, Fungus expressing wild type form of strain Mont -1 uses different types of glucose and carbon found in the vascular tissue of soybean roots to develop efficiently in contrast to its mutant strain SF18. |
complete | ||||
GO:0044123: growth of symbiont in host vascular tissue |
ECO:0000315: |
P |
The growth of strain Mont- 1 during fungal colonization was significant and efficient in colonizing its host’s vascular tissues when inoculated. |
complete | ||||
GO:0010629: negative regulation of gene expression |
ECO:0000315: |
P |
Figure 4, Gene expression was non - existent in the strain ΔSF18 during galactose metabolism compared to the positive regulation in strains Mont-1 and EctSF27. |
complete | ||||
GO:0010628: positive regulation of gene expression |
ECO:0000315: |
P |
Figure 5, “Expression of cell wall-degrading enzyme genes in Fvsnf1 mutant (ΔSF18) compared to the wild-type (Mont- 1), when grown in pectin, xylan or glucan.” As stated in article, with asterisks signifying major variances. |
complete | ||||
Notes
See also
References
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