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Chapter 13 : , Mating, Switching, and Pathogenesis in , and

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Abstract:

This chapter focuses on the relationships between mating, switching, and pathogenesis in and the comparative aspects of the mating systems in , , , and . As biofilms play such a fundamental role in both bacterial and fungal pathogenesis, this hypothesis tied together for the first time switching, mating, and pathogenesis. Daniels and coworkers assessed whether a minority of opaque cells enhanced biofilm maturation in a majority of opaque cells. It was still not known if tetraploid fusants, the product of mating, returned to the diploid state by meiosis. Candida parapsilosis may be best known for causing clinical outbreaks, but it has emerged in recent years as one of the four most common agents of yeast bloodstream infections. In phylogenetic progressions of the hemiascomycetes that incorporate events related to mating, and are positioned at the end, while branches from the base, far closer to the ancestral organism. It was, therefore, no surprise to find that the mating-type genes of were organized similarly to those of . One might argue that mating occurs only rarely, only between select strains of opposite mating types, and only under very specific environmental conditions. Due to the discovery that opaque cells signal white cells to form biofilms, the authors have suggested that mating systems in the infectious species may have been subverted into functioning in host colonization and pathogenesis.

Citation: Soll D, Daniels K. 2007. , Mating, Switching, and Pathogenesis in , and , p 215-234. In Heitman J, Kronstad J, Taylor J, Casselton L (ed), Sex in Fungi. ASM Press, Washington, DC. doi: 10.1128/9781555815837.ch13
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Figures

Image of Figure 13.1
Figure 13.1

A comparison of the mating systems of and . (A and B) The respective configurations of mating loci. (C and D) The respective steps in the mating programs and acquisition of mating competence. In panel D, the question mark next to meiosis indicates that the process has not been demonstrated.

Citation: Soll D, Daniels K. 2007. , Mating, Switching, and Pathogenesis in , and , p 215-234. In Heitman J, Kronstad J, Taylor J, Casselton L (ed), Sex in Fungi. ASM Press, Washington, DC. doi: 10.1128/9781555815837.ch13
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Image of Figure 13.2
Figure 13.2

Scanning electron micrographs of select stages in the mating process of . (A) Contact of conjugation tubes; (B) fusion of conjugation tubes; (C) daughter bud formation from conjugation bridge. Scale bar, 1 µm.

Citation: Soll D, Daniels K. 2007. , Mating, Switching, and Pathogenesis in , and , p 215-234. In Heitman J, Kronstad J, Taylor J, Casselton L (ed), Sex in Fungi. ASM Press, Washington, DC. doi: 10.1128/9781555815837.ch13
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Image of Figure 13.3
Figure 13.3

The white-opaque transition. (A) The switching system and genotype; (B) /α cells don’t switch; (C) / (or α/α) cells switch (op, opaque; wh, white); (D) SEM of white cell; (E) SEM of opaque cell; (F) TEM of pimple channel; (G) TEM of pimples around cell surface. Scale bars, 1 µm in panels D, E, and G and 100 nm in panel F.

Citation: Soll D, Daniels K. 2007. , Mating, Switching, and Pathogenesis in , and , p 215-234. In Heitman J, Kronstad J, Taylor J, Casselton L (ed), Sex in Fungi. ASM Press, Washington, DC. doi: 10.1128/9781555815837.ch13
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Image of Figure 13.4
Figure 13.4

Skin facilitates opaque-cell colonization and mating. (A) White cells poorly colonize skin. (B) Opaque cells densely colonize skin. (C) Opaque / and α/α cells mate on skin at high frequency. See Kvaal et al. ( ) and Lachke et al. ( ) for details. Scale bars, 5 µm.

Citation: Soll D, Daniels K. 2007. , Mating, Switching, and Pathogenesis in , and , p 215-234. In Heitman J, Kronstad J, Taylor J, Casselton L (ed), Sex in Fungi. ASM Press, Washington, DC. doi: 10.1128/9781555815837.ch13
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Image of Figure 13.5
Figure 13.5

α-Pheromone treatment causes shmooing and blunt conjugation tube formation in cells (A). It causes shmooing and long conjugation tube formation in (B). Scale bars, 5 µm.

Citation: Soll D, Daniels K. 2007. , Mating, Switching, and Pathogenesis in , and , p 215-234. In Heitman J, Kronstad J, Taylor J, Casselton L (ed), Sex in Fungi. ASM Press, Washington, DC. doi: 10.1128/9781555815837.ch13
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Image of Figure 13.6
Figure 13.6

A hypothesis that switching is involved in biofilm formation. The hypothesis was developed by Daniels et al. ( ) that in overlapping / and α/α populations, rare / and α/α opaque cells signal majority white cells of opposite mating types to form a biofilm that facilitates mating by stabilizing pheromone gradients.

Citation: Soll D, Daniels K. 2007. , Mating, Switching, and Pathogenesis in , and , p 215-234. In Heitman J, Kronstad J, Taylor J, Casselton L (ed), Sex in Fungi. ASM Press, Washington, DC. doi: 10.1128/9781555815837.ch13
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Image of Figure 13.7
Figure 13.7

Opaque cells induce white cells through pheromone to form a biofilm that facilitates mating. Proof for some of the steps in the hypothesis of Daniels et al. ( ). (A) α-Pheromone induces / white cells, but not / opaque cells, to form a biofilm on a plastic surface of a multiwell plate. + and −, presence and absence, respectively, of chemically synthesized 13-mer α-pheromone. (B) Facilitation of chemotropism between a rare / and α/α opaque cell in a three-dimensional biofilm. Arrows denote direction of conjugation tube growth. (C) Lack of chemotropism in the two-dimensional layer of cells at the edge of a three-dimensional biofilm. Scale bars, 5 µm.

Citation: Soll D, Daniels K. 2007. , Mating, Switching, and Pathogenesis in , and , p 215-234. In Heitman J, Kronstad J, Taylor J, Casselton L (ed), Sex in Fungi. ASM Press, Washington, DC. doi: 10.1128/9781555815837.ch13
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Image of Figure 13.8
Figure 13.8

While the great majority of natural /α strains of are virulent, the great majority of spontaneous -homozygous offspring are relatively avirulent, and natural -homozygous strains run the gamut of virulence. Virulence was measured in the mouse model for systemic infection of natural /α cells (A through C), -homozygous offspring of natural /α cells (A through C), and natural -homozygous strains (D through F). Strain names are in the upper right-hand corner of each panel. Each panel contains data for host survival over time (i.e., the percentage of injected mice still alive without signs of extreme morbidity). See Lockhart et al. ( ) and Wu et al. ( ).

Citation: Soll D, Daniels K. 2007. , Mating, Switching, and Pathogenesis in , and , p 215-234. In Heitman J, Kronstad J, Taylor J, Casselton L (ed), Sex in Fungi. ASM Press, Washington, DC. doi: 10.1128/9781555815837.ch13
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Image of Figure 13.9
Figure 13.9

While spontaneous -homozygous offspring are generated from natural /α strains by loss of one homolog of chromosome 5 followed by duplication of the retained homolog, resulting in uniparental disomy, natural -homozygous strains arise by mitotic recombination. Heterozygosities are presented along chromosome 5 for natural /α strains (A), spontaneous / offspring of natural /α strains (B), spontaneous α/α offspring of natural /α strains (C), natural / strains (D), and natural α/α strains (E). Vertical dotted lines refer to homozygosity. Details from Wu et al. ( ).

Citation: Soll D, Daniels K. 2007. , Mating, Switching, and Pathogenesis in , and , p 215-234. In Heitman J, Kronstad J, Taylor J, Casselton L (ed), Sex in Fungi. ASM Press, Washington, DC. doi: 10.1128/9781555815837.ch13
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Image of Figure 13.10
Figure 13.10

() and () can mate in vitro. (A and B) Fusion of conjugation tubes and nuclear migration to the conjugation bridge. (C and D) Nuclear fusion, daughter bud formation. (E and F) Nuclear division with one daughter nucleus migrating into daughter cell. and cells were distinguished by vital dye. See Pujol et al. ( ) for details. Scale bar, 2 µm.

Citation: Soll D, Daniels K. 2007. , Mating, Switching, and Pathogenesis in , and , p 215-234. In Heitman J, Kronstad J, Taylor J, Casselton L (ed), Sex in Fungi. ASM Press, Washington, DC. doi: 10.1128/9781555815837.ch13
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References

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