Table 2.

Summary of the fungal genes studied in glycosylation pathways.

Pathway	Function	Gene	Species	Phenotypes	Reference
		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]