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Literature summary for 2.4.1.183 extracted from

  • Beauvais, A.; Bozza, S.; Kniemeyer, O.; Formosa, C.; Formosa, C.; Balloy, V.; Henry, C.; Roberson, R.W.; Dague, E.; Chignard, M.; Brakhage, A.A.; Romani, L.; Latge, J.P.
    Deletion of the alpha-(1,3)-glucan synthase genes induces a restructuring of the conidial cell wall responsible for the avirulence of Aspergillus fumigatus (2013), PLoS Pathog., 9, e1003716.
    View publication on PubMedView publication on EuropePMC
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Protein Variants

Protein Variants Comment Organism
additional information deletion of all the three AGS genes, the ags1DELTAags2DELTAags3DELTA (agsDELTA) mutants are less virulent than the parental strain in murine model of aspergillosis, mutant phenotypes, overview. Susceptibility of the agsDELTA and parental strain conidia to antifungal molecules is similar. The resting conidia of the agsDELTA mutants are immediately recognized by the innate immune system of mice because the surface rodlet layer is masked by a layer of glycoproteins, overview Aspergillus fumigatus

Localization

Localization Comment Organism GeneOntology No. Textmining
cell wall
-
 Aspergillus fumigatus 5618
-

Organism

Organism UniProt Comment Textmining
Aspergillus fumigatus Q4WFV3 i.e. Neosartorya fumigata, gene AGS1
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Aspergillus fumigatus Q4WRQ8 i.e. Neosartorya fumigata, gene AGS3
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Aspergillus fumigatus Q4X143 i.e. Neosartorya fumigata, gene AGS2
-

Synonyms

Synonyms Comment Organism
Ags1
-
 Aspergillus fumigatus
AGS2
-
 Aspergillus fumigatus
AGS3
-
 Aspergillus fumigatus

General Information

General Information Comment Organism
malfunction deletion of all the three AGS genes results in a triple mutant that is devoid of alpha-(1,3)-glucan in its cell wall, buts growth and germination is identical to that of the parental strain in vitro. In the experimental murine aspergillosis model, this mutant is less pathogenic than the parental strain. The AGS deletion results in an extensive structural modification of the conidial cell wall, especially conidial surface where the rodlet layer is covered by an amorphous glycoprotein matrix. The surface modification is responsible for viability reduction of conidia in vivo, which explains decrease in the virulence of triple agsD mutant Aspergillus fumigatus
malfunction deletion of all the three AGS genes results in a triple mutant that is devoid of alpha-(1,3)-glucan in its cell wall, buts growth and germination is identical to that of the parental strain in vitro. In the experimental murine aspergillosis model, this mutant is less pathogenic than the parental strain. The AGS deletion results in an extensive structural modification of the conidial cell wall, especially conidial surface where the rodlet layer is covered by an amorphous glycoprotein matrix. Thie surface modification is responsible for viability reduction of conidia in vivo, which explains decrease in the virulence of triple agsD mutant Aspergillus fumigatus
physiological function the enzyme is involved in biosynthesis of alpha-1,3-glucan and the cell wall biogenesis. alpha-(1,3)-Glucan is a major cell wall component of most ascomycetous and basidiomycetous fungi, including the human pathogens. In Aspergillus fumigatus, alpha-(1,3)-glucan is a key component of the extracellular matrix, which encloses the cell wall beta-(1,3)-glucan-chitin fibrillar core Aspergillus fumigatus