Cell Wall Composition of the Mycelial and Blastospore Forms of Candida albicans

Chattaway, F. W.; Holmes, Mary R.; Barlow, Aaron

doi:10.1099/00221287-51-3-367

Cited by 275 publications

(128 citation statements)

References 15 publications

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“…Much information exists regarding the environmental factors that control the yeast-tomycelium transition (Lee et al, 1975;Mitchell & Soll, 1979;Manning & Mitchell, 1980a;Mattia et al, 1982), and several studies have also been made concerning the biochemical (Chiew et al, 1980;Sullivan et al, 1983) and antigenic differences between the two types of cells (Chattaway et al, 1968(Chattaway et al, , 1976Svedsen & Axelsen, 1972;Manning & Mitchell, 1980b, c) as well as the cytology of the process (Soll & Mitchell, 1983;Gow & Gooday, 1984). However, a deeper understanding of the biology and pathogenicity of C. albicans has been hampered by the difficulties in carrying out genetic analysis in this species.…”

Section: Introductionmentioning

confidence: 99%

Genetic Analysis of Candida albicans Morphological Mutants

Pomés¹,

Gil²,

Nombela³

1985

Microbiology

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Section: Introductionmentioning

confidence: 99%

Genetic Analysis of Candida albicans Morphological Mutants

Pomés¹,

Gil²,

Nombela³

1985

Microbiology

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“…The walls of Candida albicans and other fungi are complex structures both chemically and structurally (Chattaway et al, 1968;Cassone et al, 1973;Poulain et al, 1978). Chemically they are characterized by the presence of fl-glucans, chitin and mannoproteins.…”

Section: Introductionmentioning

confidence: 99%

Formation of a New Cell Wall by Protoplasts of Candida albicans: Effect of Papulacandin B, Tunicamycin and Nikkomycin

Elorza

Murgui²,

Rico³

et al. 1987

Microbiology

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Incorporation of polysaccharides into the walls of regenerating protoplasts of Candida albicans was followed in the presence of papulacandin B, tunicamycin and nikkomycin. With the first drug, chitin was incorporated normally whereas incorporation of glucans and mannoproteins was significantly decreased. Tunicamycin decreased incorporation of all wall polymers when added at the beginning of the regeneration process but blocked only mannan and alkaliinsoluble glucan incorporation when added after 5 h. Nikkomycin inhibited chitin synthesis, and the walls formed by the protoplasts were enriched in alkali-soluble glucan. Pulse-chase experiments suggested that a precursor-product relationship between the alkali-soluble and alkali-insoluble glucans existed in the wall. The results obtained with the antibiotics were confirmed and extended by cytological studies using wheat-germ agglutinin labelled with colloidal gold and concanavalin A-ferri tin as specific markers of chitin and mannoproteins respectively. The results support the idea that regeneration of walls by protoplasts occurs in two steps : firstly, a chitin microfibrillar skeleton is formed, and in a later step glucan-mannoprotein complexes are added to the growing structure. The chitin skeleton probably allows the orderly spatial arrangement of the other polymers giving rise to the regenerated cell wall.

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“…This fungus is capable ofdimorphic growth where growth can occur by unicellular budding or filamentous hyphal extension and branch formation (3). The hyphal cell wall has three to five times the chitin content of the yeast cell wall (4,5) and the cells have up to 10 times the in vivo chitin synthase activity (6). Three genes encoding chitin synthases have been cloned and sequenced in C. albicans (7,8,37).…”

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A hyphal-specific chitin synthase gene (CHS2) is not essential for growth, dimorphism, or virulence of Candida albicans.

Gow

Robbins

Lester

et al. 1994

Proc. Natl. Acad. Sci. U.S.A.

144

139

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In the dimorphic fungus Cad Chitin is a fibrous polymer off-1,4-N-acetylglucosamine that constitutes a major structural component of the cell wall of many species of fungi, including those species that are pathogenic in humans. Because chitin is not found in mammals and its biosynthesis is normally essential for the shape and viability of the fungal cell (1, 2), chitin synthesis is an attractive target for the design of antifungal drugs. The most common medical mycosis is caused by Candida albicans, which is a diploid organism with no sexual cycle. This fungus is capable ofdimorphic growth where growth can occur by unicellular budding or filamentous hyphal extension and branch formation (3). The hyphal cell wall has three to five times the chitin content of the yeast cell wall (4, 5) and the cells have up to 10 times the in vivo chitin synthase activity (6). Three genes encoding chitin synthases have been cloned and sequenced in C. albicans (7,8,37). Two encode chitin synthase zymogens (CHSI and CHS2), homologous to the CHS genes of Saccharomyces cerevisiae. The third chitin synthase gene, CHS3, is homologous to the S. cerevisiae CSD2 (9) gene (also called CALI) and is apparently the structural gene for an enzyme, which in S. cerevisiae, does not require proteolysis for its activity. Northern blot analysis of the C. albicans CHS genes showed that CHS2 mRNA levels were elevated in cells undergoing hyphal development, whereas the CHS1 mRNA was expressed only at low levels early in germ-tube formation (8).The role of each of the chitin synthase activities described in S. cerevisiae has been investigated by disrupting each of the relevant genes (for a review, see ref. 10). Gene disruptions are more difficult in C. albicans because the organism is constitutively diploid and because stable multiply marked strains are required for sequential gene disruptions. Sequential gene disruption of HEM3 of C. albicans has been achieved with two genetic markers (11), but host strains with sufficient markers for the disruption of more than one structural gene are not yet available. In this study, we employed the "ura-blaster" protocol originally described by Alani et al.(12) for use with S. cerevisiae, to disrupt all alleles of the hyphal-specific C. albicans CHS2 gene. This method allows the sequential disruption of target alleles. by using Ura3 auxotrophy as a single selectable marker. Because the selectable marker can be regenerated after the disruption of each allele, this method overcomes the need for multiply marked host strains and is, therefore, ideally suited for the analysis of families of genes such as the CHS genes in C. albicans. We show that the chs2 null mutant was still able to form germ tubes, albeit with a reduced chitin content compared with the isogenic wild-type parent. A prototrophic chs2-null mutant was still able to cause disease in normal and immunosuppressed mice and had a similar virulence to the parental CHS2 strain. A preliminary report of the construction of the Achs2::hisG null mutant has a...

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Cell Wall Composition of the Mycelial and Blastospore Forms of Candida albicans

Cited by 275 publications

References 15 publications

Genetic Analysis of Candida albicans Morphological Mutants

Genetic Analysis of Candida albicans Morphological Mutants

Formation of a New Cell Wall by Protoplasts of Candida albicans: Effect of Papulacandin B, Tunicamycin and Nikkomycin

A hyphal-specific chitin synthase gene (CHS2) is not essential for growth, dimorphism, or virulence of Candida albicans.

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