Protein Glycosylation in Aspergillus fumigatus Is Essential for Cell Wall Synthesis and Serves as a Promising Model of Multicellular Eukaryotic Development
Table 2
Summary of the fungal genes studied in glycosylation pathways.
Pathway
Function
Gene
Species
Phenotypes
Reference
PMI40
S. cerevisiae
The mutant only grows on media with exogenous mannose. Excess exogenous mannose leads to an accumulation of Man-6-P, which represses glycolysis, protein biosynthesis, and cell wall biogenesis
Deletion of pmi1 results in defects in cell wall integrity, conidiation, and morphology. Both lower and higher concentrations of mannose lead to a reduction in the levels of α-glucan in the cell wall and an accumulation of Man-6-P in the mutant
Mutational defects in the CWH41 gene cause severe and selective instability of glycoprotein Kre6p, a putative Golgi glucan synthase required for β-l, 6-glucan synthesis
Deletion of cwh41 leads to severe reduction in conidial formation, abnormalities of polar growth, septation and temperature-sensitive deficiency of cell wall integrity.
Deletion of msdS gene leads to a defect in N-glycan processing, as well as a reduction of cell wall components (including α-glucan, β-glucan, mannoprotein, and chitin), reduced conidiation, abnormal polarity, and septation
The Ams1p is involved in recycling macromolecular components of the cell under nutrient deprivation. Deletion of AMS1 causes no visible effect on growth or morphology
Single pmt1 mutants fail to grow in anaerobic conditions on some media. The pmt1,2,3-triple mutants grow only in osmotically stabilized medium, whereas the pmt1,2,4-and pmt2,3,4-triple mutants are not viable in any conditions
The pmt1 mutants are viable, but defective in undergoing cellular differentiation from yeast to a true hyphal growth form under some conditions. The virulence of the pmt1 null mutant is significantly attenuated. pmt1,4-double mutants are not viable. The pmt phenotypes are closely linked to alterations in cell wall components, including cell wall mannoproteins and polysaccharides
Deletion of , as well as simultaneous deletion of and , is lethal. The viable oma1D and oma4D single mutants show abnormal cell wall and septum formation
All single pmt mutants are viable but show reduced growth at elevated temperatures and defects in morphogenesis. Double deletion of pmtA/pmtC and pmtB/pmtC is lethal
Deletion of pmt1 results in temperature- sensitive phenotypes including retarded growth, cell wall defects, deficient ability of conidiation, and reduced germination
Single pmt2 or double pmt1pmt4 deletion(s) are lethal. Repression of pmt2 leads to retarded growth, cell wall defects, abnormal polarity, and reduced conidiation
Disruption of pmt4 leads to abnormal mycelial growth, poor conidiation, and abnormal polarity.
Deletion of pig-a results in a number of phenotypes including increased cell lysis, cell wall defects, abnormal hyphal growth, rapid conidial germination, aberrant conidiation, and reduced virulence