|
|
PMI40
|
S. cerevisiae
|
The pmi
− 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 |
[52] |
|
Phosphomannose isomerase (PMI) |
MAN1
|
C. neoformans
|
Disrupted MAN1 mutant displays poor capsule formation, reduced polysaccharide secretion, morphological abnormalities, and attenuated virulence |
[50] |
Mannose activation |
manA
|
A. nidulans
|
The manA1 mutant exhibits abnormal ballooning of hyphal tips and eventually ceases to grow. |
[53] |
|
|
pmi1
|
A. fumigatus
|
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 |
[54] |
|
GDP-mannose pyrophosphorylase (GMPP) |
SRB1
|
S. cerevisiae
|
Cell lysis, failure of cell separation, impaired budding and hyphal switching, clumping and flocculation, and cell wall defects |
[61] |
|
srb1
|
A. fumigatus
|
Defective cell wall and impaired polarised growth, as well as rapid germination and reduced conidiation |
[63] |
|
|
Oligosaccharyltrans- ferase (OST) |
STT3
|
S. cerevisiae
|
Essential gene |
[72, 73] |
|
stt3
|
A. fumigatus
|
Repression of the stt3 gene leads to a severe retardation of growth, a slight defect in cell wall integrity and UPR |
[39] |
|
ER Glucosidase I |
CWH41
|
S. cerevisiae
|
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 |
[23, 83, 84] |
|
cwh41
|
A. fumigatus
|
Deletion of cwh41 leads to severe reduction in conidial formation, abnormalities of polar growth, septation and temperature-sensitive deficiency of cell wall integrity. |
[37] |
N-glycosylation |
Golgi mannosidase II |
MSDS
|
S. cerevisiae
|
Disruption of t MSDS does not prevent outer chain synthesis |
[96] |
|
msdS
|
A. fumigatus
|
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 |
[97] |
|
Cytosolic/vacuolar α-mannosidase |
AMS1
|
S. cerevisiae
|
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 |
[98–101] |
|
ams1
|
A. nidulans
|
oligosaccharide catabolism; no visible effect on growth or morphology |
[102] |
|
ams1
|
A. fumigatus
|
Deletion of ams1 leads to a severe defect in conidial formation (especially at a higher temperature), abnormalities of polarity, and septation |
[103] |
|
|
|
PMT1 PMT2 PMT3 PMT4 PMT5 PMT6 PMT7
|
S. cerevisiae
|
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 |
[104, 105] |
O-glycosylation |
mannosyltransferase |
PMT1 PMT2 PMT4 PMT5 PMT6
|
C. albicans
|
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 |
[106, 107] |
|
|
oma1+, oma2+
oma4+
|
S. pombe
|
Deletion of oma2+, as well as simultaneous deletion of oma1+ and oma4+, is lethal. The viable oma1D and oma4D single mutants show abnormal cell wall and septum formation |
[108] |
|
|
PMT1 PMT2 PMT4
|
C. neoformans
|
Pmt4p is essential for morphogenesis and virulence. PMT2 is an essential gene, and the double pmt1pmt4 deletion is synthetically lethal |
[109, 110] |
|
|
pmtA pmtB pmtC
|
A. nidulans
|
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 |
[111, 112] |
|
|
pmt1 pmt2 pmt4
|
A. fumigatus
|
Deletion of pmt1 results in temperature- sensitive phenotypes including retarded growth, cell wall defects, deficient ability of conidiation, and reduced germination |
[113–115] |
|
|
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. |
|
GPI-anchoring |
Glycosylphosphatidyl-inositol-N-acetyl- glucosaminyltrans- ferase (GPI-GnT) |
GPI3
|
S. cerevisiae
|
A gpi3 temperature-sensitive mutant is lethal at 37°C |
[116, 117] |
gpig-1
|
N. crassa
|
Temperature-sensitive phenotypes |
[118] |
pig-a
|
A. fumigatus
|
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 |
[119] |