1887

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

MyBook is a cheap paperback edition of the original book and will be sold at uniform, low price.

Ebook: Choose a downloadable PDF or ePub file. Chapter is a downloadable PDF file. File must be downloaded within 48 hours of purchase

Buy this Chapter
Digital (?) $15.00

Preview this chapter:
Zoom in
Zoomout

, Mating, Switching, and Pathogenesis in , and , Page 1 of 2

| /docserver/preview/fulltext/10.1128/9781555815837/9781555814212_Chap13-1.gif /docserver/preview/fulltext/10.1128/9781555815837/9781555814212_Chap13-2.gif

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
Highlighted Text: Show | Hide
Loading full text...

Full text loading...

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
Permissions and Reprints Request Permissions
Download as Powerpoint
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
Permissions and Reprints Request Permissions
Download as Powerpoint
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
Permissions and Reprints Request Permissions
Download as Powerpoint
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
Permissions and Reprints Request Permissions
Download as Powerpoint
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
Permissions and Reprints Request Permissions
Download as Powerpoint
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
Permissions and Reprints Request Permissions
Download as Powerpoint
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
Permissions and Reprints Request Permissions
Download as Powerpoint
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
Permissions and Reprints Request Permissions
Download as Powerpoint
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
Permissions and Reprints Request Permissions
Download as Powerpoint
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
Permissions and Reprints Request Permissions
Download as Powerpoint

References

/content/book/10.1128/9781555815837.ch13
1. Anderson, J. M., and, D. R. Soll. 1987. Unique phenotype of opaque cells in the white-opaque transition of Candida albicans. J. Bacteriol. 169:55795588.
2. Anderson, J.,, R. Mihalik, and, D. R. Soll. 1990. Ultrastructure and antigenicity of the unique cell wall pimple of the Candida opaque phenotype. J. Bacteriol. 172:224235.
3. Anderson, J. B.,, C. Wickens,, M. Khan,, L. E. Cowen,, N. Federspiel,, T. Jones, and, L. M. Kohn. 2001. Infrequent genetic exchange and recombination in the mitochondrial genome of Candida albicans. J. Bacteriol. 183:865872.
4. Bardwell, L. 2005. A walk-through of the yeast mating pheromone response pathway. Peptides 26:339350.
5. Barns,, S. M., D. J. Lane,, M. L. Sogin,, C. Bibeau, and, W. G. Weisburg. 1991. Evolutionary relationships among pathogenic Candida species and relatives. J. Bacteriol. 173:22502255.
6. Bennett, R. J., and, A. D. Johnson. 2003. Completion of a parasexual cycle in Candida albicans by induced chromosome loss in tetraploid strains. EMBO J. 22:25052515.
7. Bennett, R. J.,, M. A. Uhl,, M. G. Miller, and, A. D. Johnson. 2003. Identification and characterization of a Candida albicans mating pheromone. Mol. Cell. Biol. 23:81898201.
8. Bennett, R. J.,, M. G. Miller,, P. R. Chua,, M. E. Maxon, and, A. D. Johnson. 2005. Nuclear fusion occurs during mating in Candida albicans and is dependent on the KAR3 gene. Mol. Microbiol. 55:10461059.
9. Blaschke-Hellmessen, R. 1996. Fluconazole and itraconazole susceptibility testing with clinical yeast isolates and algae of the genus Prototheca by means of the Etest. Mycoses 39(Suppl. 2):3943.
10. Blignaut,, E., C. Pujol,, S. Lockhart,, S. Joly, and, D. R. Soll. 2002. Ca3 fingerprinting of Candida albicans isolates from human immunodeficiency virus-positive individuals reveals a new clade in South Africa. J. Clin. Microbiol. 40:826836.
11. Boerlin, P.,, F. Boerlin-Petzold,, C. Durussel,, M. Ado,, J.-L. Pagani,, J.-P. Chave, and, J. Bille. 1995. Cluster of oral atypical Candida albicans isolates in a group of human immunodeficiency virus-positive drug users. J. Clin. Microbiol. 33:11291135.
12. Brockert, P. J.,, S. A. Lachke,, T. Srikantha,, C. Pujol,, R. Galask, and, D. R. Soll. 2003. Phenotypic switching and mating type switching of Candida glabrata at sites of colonization. Infect. Immun. 12:71097118.
13. Butler, G.,, C. Kenny,, A. Fagan,, C. Kurischko,, C. Gaillardin, and, K. H. Wolfe. 2004. Evolution of the MAT locus and its Ho endonuclease in yeast species. Proc. Natl. Acad. Sci. USA 101:16321637.
14. Cai, J.,, I. N. Roberts, and, M. D. Collins. 1996. Phylogenetic relationships among members of the ascomycetous yeast genera Brettanomyces, Debaryomyces, Dekkera, and Kluyveromyces deduced by small-subunit rRNA gene sequences. Int. J. Syst. Bacteriol. 46:542549.
15. Chen, J.,, J. Chen,, S. Lane, and, H. Liu. 2002. A conserved mitogen-activated protein kinase pathway is required for mating in Candida albicans. Mol. Microbiol. 46:13351344.
16. Coleman, D. C.,, D. J. Sullivan,, D. E. Bennett,, G. P. Moran,, H. J. Barry, and, D. B. Shanley. 1997. Candidiasis: the emergence of a novel species Candida dubliniensis. AIDS 11:557567.
17. Csank, C., and, K. Haynes. 2000. Candida glabrata displays pseudohyphal growth. FEMS Microbiol. Lett. 189:115120.
18. Daniels, K. J.,, S. R. Lockhart,, P. Sundstrum, and, D. R. Soll. 2003. During Candida albicans mating, the adhesin Hwp1 and the first daughter bud localize to the a/a portion of the conjugation bridge. Mol. Biol. Cell 14:49204930.
19. Daniels, K. J.,, T. Srikantha,, S. R. Lockhart,, C. Pujol, and, D. R. Soll. 2006. Opaque cells signal white cells to form biofilms in Candida albicans. EMBO J. 25:22402252.
20. Diezmann, S.,, C. J. Cox,, G. Schonian,, R. J. Vilgalys, and, T. G. Mitchell. 2004. Phylogeny and evolution of medical species of Candida and related taxa: a multigenic analysis. J. Clin. Microbiol. 42:56245635.
21. Dodgson, A. R.,, C. Pujol,, D. W. Denning,, D. R. Soll, and, A. J. Fox. 2003. Multilocus sequence typing of Candida glabrata reveals geographically enriched clades. J. Clin. Microbiol. 41:57095717.
22. Edmond, M. B.,, S. E. Wallace,, D. K. McClish,, M. A. Pfaller,, R. N. Jones, and, R. P. Wenzel. 1999. Nosocomial bloodstream infections in United States hospitals: a threeyear analysis. Clin. Infect. Dis. 29:239244.
23. Fortun, J.,, A. Lopez-San Roman,, J. J. Velasco,, A. Sanchez-Sousa,, E. de Vicente,, J. Nuno,, C. Quereda,, R. Barcena,, G. Monge,, A. Candela,, A. Honrubia, and, A. Guerrero. 1997. Selection of Candida glabrata strains with reduced susceptibility to azoles in four liver transplant patients with invasive candidiasis. Eur. J. Clin. Microbiol. Infect. Dis. 16:314318.
24. Graser, Y.,, M. Volovsek,, J. Arrington,, G. Schonian,, W. Presber,, T. G. Mitchell, and, R. Vilgalys. 1996. Molecular markers reveal that population structure of the human pathogen Candida albicans exhibits both clonality and recombination. Proc. Natl. Acad. Sci. USA 93:1247312477.
25. Haber, J. E. 1998. Mating-type gene switching in Saccharomyces cerevisiae. Annu. Rev. Genet. 32:561599.
26. Hawser,, S. P., and L. J. Douglas. 1994. Biofilm formation by Candida species on the surface of catheter materials in vitro. Infect. Immun. 62:915921.
27. Herskowitz, I.,, J. Rine, and, J. N. Strathern. 1992. Mating-type determination and mating-type interconversion in Saccharomyces cerevisiae, p. 583–656. In E. W. Jones,, J. R. Pringle, and, J. R. Broach (ed.), The Molecular and Cellular Biology of the Yeast Saccharomyces. Cold Spring Harbor Laboratory Press, Cold Spring Harbor, NY.
28. Hitchcock, C. A.,, G. W. Pye,, P. F. Troke,, E. M. Johnson, and, D. W. Warnock. 1993. Fluconazole resistance in Candida glabrata. Antimicrob. Agents. Chemother. 37:19621965.
29. Huang, G.,, H. Wang,, S. Chou,, X. Nie,, J. Chen, and, H. Liu. 2006. Bistable expression of WOR1, a master regulator of white-opaque switching in Candida albicans. Proc. Natl. Acad. Sci. USA 103:1281312818.
30. Hube, B.,, M. Monod,, D. Schofield,, A. Brown, and, N. Gow. 1994. Expression of seven members of the gene family encoding aspartyl proteinases in Candida albicans. Mol. Microbiol. 14:8799.
31. Hull, C. M., and, A. D. Johnson. 1999. Identification of a mating type-like locus in the asexual pathogenic yeast Candida albicans. Science 285:12711275.
32. Hull, C. M.,, R. M. Raisner, and, A. D. Johnson. 2000. Evidence for mating of the “asexual” yeast Candida albicans in a mammalian host. Science 289:307310.
33. Ibrahim, A. S.,, B. B. Magee,, D. C. Sheppard,, M. Yang,, S. Kauffman,, J. Becker,, J. E. Edwards,, Jr., and P. T. Magee. 2005. Effects of ploidy and mating type on virulence of Candida albicans. Infect. Immun. 73:73667374.
34. Janbon, G.,, F. Sherman, and, E. Rustcheko. 1999. Appearance and properties of L-sorbose-utilizing mutants of Candida albicans obtained on a selective plate. Genetics 153:653664.
35. Joly, S.,, C. Pujol, and, D. R. Soll. 2002. Microevolutionary changes and chromosomal translocations are more frequent at RPS loci in Candida dubliniensis than in Candida albicans. Infect. Genet. Evol. 2:1937.
36. Kvaal, C. A.,, T. Srikantha, and, D. R. Soll. 1997. Misexpression of the white phase-specific gene WH11 in the opaque phase of Candida albicans affects switching and virulence. Infect. Immun. 65:44684475.
37. Kvaal, C.,, S. A. Lachke,, T. Srikantha,, K. Daniels,, J. McCoy, and, D. R. Soll. 1999. Misexpression of the opaque phase-specific gene PEP1 (SAP1) in the white phase of Candida albicans confers increased virulence in a mouse model of cutaneous infection. Infect. Immun. 67:66526662.
38. Lachke, S. A.,, S. Joly,, K. Daniels, and, D. R. Soll. 2002. Phenotypic switching and filamentation in Candida glabrata. Microbiology 148:26612674.
39. Lachke, S. A.,, S. R. Lockhart,, K. J. Daniels, and, D. R. Soll. 2003. Skin facilitates Candida albicans mating. Infect. Immun. 71:49704976.
40. Lachke, S. A.,, T. Srikantha, and, D. R. Soll. 2003. The regulation of EFG1 in white-opaque switching in Candida albicans involves overlapping promoters. Mol. Microbiol. 48:523536.
41. Lachke, S. A.,, T. Srikantha,, L. Tsai,, K. Daniels, and, D. R. Soll. 2000. Phenotypic switching in Candida glabrata involves phase-specific regulation of the metallotheionein gene MT-II and the newly discovered hemolysin gene HLP. Infect. Immun. 68:884895.
42. Lan, C. Y.,, G. Newport,, L. A. Murillo,, T. Jones,, S. Scherer,, R. W. Davis, and, N. Agabian. 2002. Metabolic specialization associated with phenotypic switching in Candida albicans. Proc. Natl. Acad. Sci. USA 99:1490714912.
43. Legrand, M.,, P. Lephart,, A. Forsche,, F.-M. C. Mueller,, T. Walsh,, P. T. Magee, and, B. B. Magee. 2004. Homozygosity at the MTL locus in clinical strains of Candida albicans: karyotypic rearrangements and tetraploid formation. Mol. Microbiol. 52:14511462.
44. Lockhart, S. R.,, C. Pujol,, K. Daniels,, M. Miller,, A. Johnson, and, D. R. Soll. 2002. In Candida albicans, white-opaque switchers are homozygous for mating type. Genetics 162:737745.
45. Lockhart, S. R.,, K. J. Daniels,, R. Zhao,, D. Wessels, and, D. R. Soll. 2003. Cell biology of mating in Candida albicans. Eukaryot. Cell 2:4961.
46. Lockhart, S. R.,, M. Nguyen,, T. Srikantha, and, D. R. Soll. 1998. A MADS box protein consensus binding site is necessary and sufficient for activation of the opaque-phase specific gene OP4 of Candida albicans. J. Bacteriol. 180:66076616.
47. Lockhart, S. R.,, S. Joly,, K. Vargas,, J. Swails-Wenger,, L. Enger, and, D. R. Soll. 1999. Natural defenses against Candida colonization breakdown in the oral cavities of the elderly. J. Dent. Res. 78:857868.
48. Lockhart, S. R.,, W. Wu,, J. B. Radke, and, D. R. Soll. 2005. Increased virulence and competitive advantage of a/α over a/a or α/α offspring conserves the mating system of Candida albicans. Genetics 169:18831890.
49. Lockhart, S. R.,, R. Zhao,, K. J. Daniels, and, D. R. Soll. 2003. α-Pheromoneinduced “shmooing” and gene regulation require white-opaque switching during Candida albicans mating. Eukaryot. Cell 2:847855.
50. Logue, M. E.,, S. Wong,, K. H. Wolfe, and, G. Butler. 2005. A genome sequence survey shows that the pathogenic yeast Candida parapsilosis has a defective MTLa1 allele at its mating type locus. Eukaryot. Cell 4:10091017.
51. Magee, B. B., and, P. T. Magee. 2000. Induction of mating in Candida albicans by construction of MTLa and MTLalpha strains. Science 289:310313.
52. Magee, B. B.,, M. Legrand,, A. M. Alarco,, M. Raymond, and, P. T. Magee. 2002. Many of the genes required for mating in Saccharomyces cerevisiae are also required for mating in Candida albicans. Mol. Microbiol. 46:13451351.
53. Marichal, P.,, H. Vanden Bossche,, F. C. Odds,, G. Nobels,, D. W. Warnock,, V. Timmerman,, C. Van Broeckhoven,, S. Fay, and, P. Mose-Larsen. 1997. Molecular biological characterization of an azole-resistant Candida glabrata isolate. Antimicrob. Agents Chemother. 41:22292237.
54. McCullough, M.,, B. Ross, and, P. Reade. 1995. Characterization of genetically distinct subgroup of Candida albicans strains isolated from oral cavities of patients infected with human immunodeficiency virus. J. Clin. Microbiol. 33:696700.
55. Miller, M. G., and, A. D. Johnson. 2002. White-opaque switching in Candida albicans is controlled by mating-type locus homeodomain proteins and allows efficient mating. Cell 110:293302.
56. Moran, G.,, C. Stokes,, S. Thewes,, B. Hube,, D. C. Coleman, and, D. Sullivan. 2004. Comparative genomics using Candida albicans DNA microarrays reveals absence and divergence of virulence-associated genes in Candida dubliniensis. Microbiology 150:33633382.
57. Morrow, B.,, T. Srikantha, and, D. R. Soll. 1992. Transcription of the gene for a pepsinogen, PEP1, is regulated by white-opaque switching in Candida albicans. Mol. Cell. Biol. 12:29973005.
58. Morrow, B.,, T. Srikantha,, J. Anderson, and, D. R. Soll. 1993. Coordinate regulation of two opaque-specific genes during white-opaque switching in Candida albicans. Infect. Immun. 61:18231828.
59. Mukherjee, P. K.,, G. Zhou,, R. Munyon, and, M. A. Ghannoum. 2005. Candida biofilm: a well-designed protected environment. Med. Mycol. 43:191208.
60. Odds, F. C. 1988. Candida and Candidosis, 2nd ed. Bailliere Tindall, London, England.
61. Pfaller, M. A.,, D. J. Diekema,, R. N. Jones,, H. S. Sader,, A. C. Fluit,, R. J. Hollis, and, S. A. Messer. 2001. International surveillance of bloodstream infections due to Candida species: frequency and occurrence and in vitro susceptibilities to fluconazole, ravuconazole, and viriconazole of isolates collected from 1997 through 1999 in the SENTRY antimicrobial surveillance program. J. Clin. Microbiol. 39:32543259.
62. Pujol, C.,, A. Dodgson, and, D. R. Soll. 2005. Population genetics of ascomycetes pathogenic to humans and animals, p. 149–188. In J.-P. Xu (ed.), Evolutionary Genetics of Fungi. Horizon Scientific Press, Norfolk, United Kingdom.
63. Pujol, C.,, K. J. Daniels,, T. Srikantha,, S. R. Lockhart,, J. Geiger, and, D. R. Soll. 2004. The two closely related species Candida albicans and Candida dubliniensis can mate. Eukaryot. Cell 3:10151027.
64. Pujol, C.,, F. Renaud,, M. Mallie,, T. de Meeus, and J. M. Bastide. 1997. Atypical strains of Candida albicans recovered from AIDS patients. J. Med. Vet. Mycol. 35:115121.
65. Pujol, C.,, J. Reynes,, F. Renaud,, M. Raymond,, M. Tibayrenc,, F. J. Ayala,, F. Janbon,, M. Mallie, and, J. M. Bastide. 1993. The yeast Candida albicans has a clonal mode of reproduction in a population of infected human immunodeficiency virus-positive patients. Proc. Natl. Acad. Sci. USA 90:94569459.
66. Pujol, C.,, S. Joly,, S. R. Lockhart,, S. Noel,, M. Tibayrenc, and, D. R. Soll. 1997. Parity among the randomly amplified polymorphic DNA method, multilocus enzyme electrophoresis, and Southern blot hybridization with the moderately repetitive DNA probe Ca3 for fingerprinting Candida albicans. J. Clin. Microbiol. 35:23482358.
67. Rikkerink, E. H.,, B. B. Magee, and, P. T. Magee. 1988. Opaque-white phenotype transition: a programmed morphological transition in Candida albicans. J. Bacteriol. 170:895899.
68. Roberts, C. J.,, B. Nelson,, M. J. Matron,, R. Stoughton,, M. R. Meyer,, H. A. Bennett,, Y. D. He,, H. Dai,, W. L. Walker,, T. R. Hughes,, M. Tyers,, C. Boone, and, S. H. Friend. 2000. Signaling and circuitry of multiple MAPK pathways revealed by a matrix of global gene expression profiles. Science 287:873880.
69. Schwartz, M. A., and, H. D. Madhani. 2004. Principles of MAP kinase signaling specificity in Saccharomyces cerevisiae. Annu. Rev. Genet. 38:725748.
70. Slutsky, B.,, M. Staebell,, J. Anderson,, L. Risen,, M. Pfaller, and, D. R. Soll. 1987. “White-opaque transition”: a second high-frequency switching system in Candida albicans. J. Bacteriol. 169:189197.
71. Soll, D. R. 2003. Candida albicans, p. 165–201. In A. Craig and, A. Scherf (ed.), Antigenic Variation. Academic Press, London, United Kingdom.
72. Soll, D. R. 2004. Mating-type locus homozygosis, phenotypic switching and mating: a unique sequence of dependencies in Candida albicans. Bioessays 26:1020.
73. Soll, D. R. The evolution of a mating system uniquely dependent upon switching and pathogenesis in Candida albicans. In F. Basquero,, C. Nombela,, G. H. Cassell, and, J. A. Gutierrez (ed.), Introduction to the Evolutionary Biology of Bacterial and Fungal Pathogens, in press.
74. Srikantha, T.,, A. R. Borneman,, K. J. Daniels,, C. Pujol,, W. Wu,, M. R. Seringhaus,, M. Gerstein,, S. Yi,, M. Snyder, and, D. R. Soll. TOS9 regulates white-opaque switching in Candida albicans. Eukaryot. Cell 5:16741687.
75. Srikantha, T., and, D. R. Soll. 1993. A white-specific gene in the white-opaque switching system of Candida albicans. Gene 131:5360.
76. Srikantha, T.,, A. Chandrasekhar, and, D. R. Soll. 1995. Functional analysis of the promoter of the phase-specific WH11 gene of Candida albicans. Mol. Cell. Biol. 15:17971805.
77. Srikantha, T.,, L. Tsai, and, D. R. Soll. 1997. The WH11 gene of Candida albicans is regulated in two distinct developmental programs through the same transcription activation sequences. J. Bacteriol. 179:38373844.
78. Srikantha, T.,, S. A. Lachke, and, D. R. Soll. 2003. Three mating type-like loci in Candida glabrata. Eukaryot. Cell 2:328340.
79. Sullivan, D. J.,, K. Haynes,, J. Bille,, P. Boerlin,, L. Rodero,, S. Lloyd,, M. Henman, and, D. Coleman. 1997. Widespread geographic distribution of oral Candida dubliniensis strains in human immunodeficiency virus-infected individuals. J. Clin. Microbiol. 35:960964.
80. Tavanti, A.,, A. D. Davidson,, M. J. Fordyce,, N. A. R. Gow,, M. C. J. Maiden, and, F. C. Odds. 2005. Population structure and properties of Candida albicans as determined by multilocus sequence typing. J. Clin. Microbiol. 43:56015613.
81. Tsong, A. E.,, M. G. Miller,, R. M. Raisner, and, A. D. Johnson. 2003. Evolution of a combinatorial transcriptional circuit: a case study in yeasts. Cell 115:389399.
82. Tzung, K.-W.,, R. M. Williams,, S. Scherer,, N. Federspiel,, T. Jones,, N. Hansen,, V. Bivolarevic,, L. Huizar,, C. Komp,, R. Surzycki,, R. Tamse,, R. W. Davis, and, N. Agabian. 2001. Genomic evidence for a complete sexual cycle in Candida albicans. Proc. Natl. Acad. Sci. USA 98:32493253.
83. Whelan, W. L., and, K. J. Kwon-Chung. 1988. Auxotrophic heterozygosities and the ploidy of Candida parapsilosis and Candida krusei. J. Med. Vet. Mycol. 26:163171.
84. White, T. C.,, H. Miyasaki, and, N. Agabian. 1993. Three distinct secreted aspartyl proteinases in Candida albicans. J. Bacteriol. 175:61266135.
85. Wong, S.,, M. A. Fares,, W. Zimmermann,, G. Butler, and, K. H. Wolfe. 2003. Evidence from comparative genomics for a complete sexual cycle in the ‘asexual’ pathogenic yeast Candida glabrata. Genome Biol. 4:R10.
86. Wu, W.,, C. Pujol,, S. R. Lockhart, and, D. R. Soll. 2005. Mechanisms of mating type homozygosis in C. albicans. Genetics 169:13111327.
87. Wu, W.,, S. R. Lockhart,, C. Pujol,, T. Srikantha, and, D. R. Soll. 2007. Heterozygosity of genes on the sex chromosome regulates Candida albicans virulence. Mol. Microbiol., in press.
88. Zhao, R.,, K. J. Daniels,, S. R. Lockhart,, K. M. Yeater,, L. L. Hoyer, and, D. R. Soll. 2005. Unique aspects of gene expression during Candida albicans mating and possible G1 dependency. Eukaryot. Cell 4:11751190.
89. Zordan, R. E.,, D. J. Galgoczy, and, A. D. Johnson. 2006. Epigenetic properties of white-opaque switching in Candida albicans are based on a self-sustaining transcriptional feedback loop. Proc. Natl. Acad. Sci. USA 103:1280712812.

This is a required field
Please enter a valid email address
Please check the format of the address you have entered.
Approval was a Success
Invalid data
An Error Occurred
Approval was partially successful, following selected items could not be processed due to error