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Chapter 21 : History of the Mating Types in

Author: Flora Banuett1
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Affiliations: 1: Department of Biological Sciences, California State University, 1250 Bellflower Bvd., Long Beach, CA 90840
Content Type: Monograph
Publication Year: 2007

Category: Fungi and Fungal Pathogenesis

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Abstract:

This chapter presents some general features of and a synopsis of its life cycle. The life cycle of is characterized by three cell types: a cigar-shaped haploid, unicellular form that divides by budding and is nonpathogenic; a dikaryotic, filamentous form that grows at the tip cell and is pathogenic; and a diploid spore, the teliospore, formed within the tumors induced by the fungus, that is not capable of vegetative growth but germinates and undergoes meiosis to produce the haploid yeast-like form. Heterothallism and Sex Factors Stakman and Christensen demonstrated for the first time that is heterothallic. Six mutants designated (three , two , and one ) were obtained, all of which induced tumors and produced teliospores when inoculated with their progenitors, with themselves and with each other, and thus behave as “universal” alleles. The locus of was the first multiallelic mating-type locus cloned and understood at the molecular level and provided a framework in which to understand the more complex A multiallelic mating-type locus of other basidiomycetes. Strains with an inactive gene for the pheromone precursor can respond to the pheromone produced by cells of opposite mating type but they cannot induce a response in cells of opposite mating type, and strains with an inactive receptor gene can induce a response in cells of opposite mating type but cannot respond to cells of opposite mating type.

Citation: Banuett F. 2007. History of the Mating Types in , p 351-375. In Heitman J, Kronstad J, Taylor J, Casselton L (ed), Sex in Fungi. ASM Press, Washington, DC. doi: 10.1128/9781555815837.ch21
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History of the Mating Types in Ustilago maydis
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Citation: Banuett F. 2007. History of the Mating Types in , p 351-375. In Heitman J, Kronstad J, Taylor J, Casselton L (ed), Sex in Fungi. ASM Press, Washington, DC. doi: 10.1128/9781555815837.ch21
/content/10.1128/9781555815837.ch21.ch21fig01
Figure 21.1
Morphological transitions in the life cycle of . exhibits three forms (cell types) during its life cycle: a haploid unicellular form; a filamentous dikaryon; and a diploid spore, the teliospore (reviewed in references , and ). The transition from one form to the other entails conjugation, karyogamy, and meiosis. These processes are accompanied by changes in ploidy, growth habit, and pathogenicity (see references , and for details). These morphological transitions are governed by two unlinked mating-type loci, and , by environment, by nutrients, and possibly by plant signals (reviewed in references , and ). (From reference , with permission.)
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Figure 21.1

Morphological transitions in the life cycle of . exhibits three forms (cell types) during its life cycle: a haploid unicellular form; a filamentous dikaryon; and a diploid spore, the teliospore (reviewed in references , and ). The transition from one form to the other entails conjugation, karyogamy, and meiosis. These processes are accompanied by changes in ploidy, growth habit, and pathogenicity (see references , and for details). These morphological transitions are governed by two unlinked mating-type loci, and , by environment, by nutrients, and possibly by plant signals (reviewed in references , and ). (From reference , with permission.)

Citation: Banuett F. 2007. History of the Mating Types in , p 351-375. In Heitman J, Kronstad J, Taylor J, Casselton L (ed), Sex in Fungi. ASM Press, Washington, DC. doi: 10.1128/9781555815837.ch21
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Figure 21.2
Teliospore germination and meiosis. The teliospore is a diploid spore, resistant to adverse environmental conditions. It is formed within the tumors following a discrete developmental program during which changes in morphology take place and karyogamy occurs ( ). Upon germination, a short filament (the promycelium) emerges, into which the diploid nucleus migrates and undergoes meiosis to form a septate promycelium consisting of four haploid cells ( ) (A). Clones of these primary meiotic products arise by budding to produce yeast-like cells (panel A), which can be removed with the aid of a micromanipulator for single tetrad analysis (panel B). Alternatively, the teliospore is allowed to germinate and form a microcolony, which is then resuspended in water and spread on an agar surface (panel C).
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Figure 21.2

Teliospore germination and meiosis. The teliospore is a diploid spore, resistant to adverse environmental conditions. It is formed within the tumors following a discrete developmental program during which changes in morphology take place and karyogamy occurs ( ). Upon germination, a short filament (the promycelium) emerges, into which the diploid nucleus migrates and undergoes meiosis to form a septate promycelium consisting of four haploid cells ( ) (A). Clones of these primary meiotic products arise by budding to produce yeast-like cells (panel A), which can be removed with the aid of a micromanipulator for single tetrad analysis (panel B). Alternatively, the teliospore is allowed to germinate and form a microcolony, which is then resuspended in water and spread on an agar surface (panel C).

Citation: Banuett F. 2007. History of the Mating Types in , p 351-375. In Heitman J, Kronstad J, Taylor J, Casselton L (ed), Sex in Fungi. ASM Press, Washington, DC. doi: 10.1128/9781555815837.ch21
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Figure 21.3
The fuzz reaction of haploid and Fuz– diploid strains on charcoal agar. Haploid and diploid strains carrying different and alleles produce a white fuzziness due to the formation of filaments in combination with haploid tester strains ( ). Saturated cultures of tester strains (vertical lines) were cross-streaked versus haploid (top four horizontal lines) and Fuz– diploids (bottom four horizontal lines). The testers are, from left to right, (FB1), (FB2), (FB6b), and (FB6a). The horizontal lines represent, from top to bottom, strains , , , , and (class I; FB-D12-3); (class II; FB-D11-21); (class III; FB-D11-7); and (class IV; FB-D12-11) (see reference for further details). (From reference , with permission.)
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Figure 21.3

The fuzz reaction of haploid and Fuz– diploid strains on charcoal agar. Haploid and diploid strains carrying different and alleles produce a white fuzziness due to the formation of filaments in combination with haploid tester strains ( ). Saturated cultures of tester strains (vertical lines) were cross-streaked versus haploid (top four horizontal lines) and Fuz– diploids (bottom four horizontal lines). The testers are, from left to right, (FB1), (FB2), (FB6b), and (FB6a). The horizontal lines represent, from top to bottom, strains , , , , and (class I; FB-D12-3); (class II; FB-D11-21); (class III; FB-D11-7); and (class IV; FB-D12-11) (see reference for further details). (From reference , with permission.)

Citation: Banuett F. 2007. History of the Mating Types in , p 351-375. In Heitman J, Kronstad J, Taylor J, Casselton L (ed), Sex in Fungi. ASM Press, Washington, DC. doi: 10.1128/9781555815837.ch21
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Figure 21.4
The molecular structure and organization of the locus. The locus is the major determinant of filamentous growth and pathogencity (reviewed in references , and ) and is estimated to have 25 naturally occurring alleles ( ), each of which consists of two divergently transcribed genes, and , separated by an intergenic region of approximately 200 bp ( ). Each gene codes for a polypeptide containing a homeodomain-related motif ( ). The bW and bE polypeptides have the same structural organization, a variable region at the amino terminus and a constant region for the remainder of the polypeptide, but show no similarity except for the homeodomain region ( ). The active b protein is found only in the dikaryon and consists of a bW and a bE subunit encoded by different alleles, for example, bW1-bE2 or bW2-bE1 ( ). Each dikaryon has two different active heterodimers, but only one is necessary for activity ( ). The variable region is the specificity determinant and controls dimerization of these polypeptides ( ). The homeodomain of both bE and bW is required for activity ( ). (From reference with permission.)
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Figure 21.4

The molecular structure and organization of the locus. The locus is the major determinant of filamentous growth and pathogencity (reviewed in references , and ) and is estimated to have 25 naturally occurring alleles ( ), each of which consists of two divergently transcribed genes, and , separated by an intergenic region of approximately 200 bp ( ). Each gene codes for a polypeptide containing a homeodomain-related motif ( ). The bW and bE polypeptides have the same structural organization, a variable region at the amino terminus and a constant region for the remainder of the polypeptide, but show no similarity except for the homeodomain region ( ). The active b protein is found only in the dikaryon and consists of a bW and a bE subunit encoded by different alleles, for example, bW1-bE2 or bW2-bE1 ( ). Each dikaryon has two different active heterodimers, but only one is necessary for activity ( ). The variable region is the specificity determinant and controls dimerization of these polypeptides ( ). The homeodomain of both bE and bW is required for activity ( ). (From reference with permission.)

Citation: Banuett F. 2007. History of the Mating Types in , p 351-375. In Heitman J, Kronstad J, Taylor J, Casselton L (ed), Sex in Fungi. ASM Press, Washington, DC. doi: 10.1128/9781555815837.ch21
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Figure 21.5
Amino acid sequence comparison of bE and bW polypeptides. The amino acid sequences of seven bE and four bW polypeptides are shown ( ). The variable region of bE and bW encompasses the first 110 and 140 amino acids, respectively. The remainder of the polypeptide is the constant region (not shown in its entirety) and contains the homeodomain. The three helices of the homeodomain are shaded. The homeodomain of bE belongs to the atypical class of homeodomains, whereas that of bW belongs to the typical class (see reference ).
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Figure 21.5

Amino acid sequence comparison of bE and bW polypeptides. The amino acid sequences of seven bE and four bW polypeptides are shown ( ). The variable region of bE and bW encompasses the first 110 and 140 amino acids, respectively. The remainder of the polypeptide is the constant region (not shown in its entirety) and contains the homeodomain. The three helices of the homeodomain are shaded. The homeodomain of bE belongs to the atypical class of homeodomains, whereas that of bW belongs to the typical class (see reference ).

Citation: Banuett F. 2007. History of the Mating Types in , p 351-375. In Heitman J, Kronstad J, Taylor J, Casselton L (ed), Sex in Fungi. ASM Press, Washington, DC. doi: 10.1128/9781555815837.ch21
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Figure 21.6
Deletion analysis of the locus. The or or both genes were deleted in haploid strains ( ), and the resulting mutants were tested for b activity (filament formation [Fuz phenotype] and tumor induction [Tum phenotype]) by cospotting on charcoal agar and inoculation into corn plants, respectively. The strains listed under strain 1 are derivatives of , and those under strain 2 are derivatives of . Mixtures of wild-type and strains result in a Fuz Tum phenotype (row 1). Deletion of one gene or one gene in one of the partners does not affect activity (rows 2 and 3, respectively). On the other hand, activity is abolished by deletion of both and in one of the partners (row 4), both and genes in both partners (row 5), in both partners (row 6), or in both partners (row 7). In contrast, deletion of in one partner and in the other (row 8) or of in one partner and in the other (row 9) does not abolish activity and demonstrates that and from different alleles are necessary for activity ( ). The dikaryon contains two active heterodimers, but only one is necessary for function (rows 8 and 9).
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Figure 21.6

Deletion analysis of the locus. The or or both genes were deleted in haploid strains ( ), and the resulting mutants were tested for b activity (filament formation [Fuz phenotype] and tumor induction [Tum phenotype]) by cospotting on charcoal agar and inoculation into corn plants, respectively. The strains listed under strain 1 are derivatives of , and those under strain 2 are derivatives of . Mixtures of wild-type and strains result in a Fuz Tum phenotype (row 1). Deletion of one gene or one gene in one of the partners does not affect activity (rows 2 and 3, respectively). On the other hand, activity is abolished by deletion of both and in one of the partners (row 4), both and genes in both partners (row 5), in both partners (row 6), or in both partners (row 7). In contrast, deletion of in one partner and in the other (row 8) or of in one partner and in the other (row 9) does not abolish activity and demonstrates that and from different alleles are necessary for activity ( ). The dikaryon contains two active heterodimers, but only one is necessary for function (rows 8 and 9).

Citation: Banuett F. 2007. History of the Mating Types in , p 351-375. In Heitman J, Kronstad J, Taylor J, Casselton L (ed), Sex in Fungi. ASM Press, Washington, DC. doi: 10.1128/9781555815837.ch21
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Figure 21.7
chimeric alleles delimit the specificity region. Chimeras between and or between and were generated by homologous recombination at the locus ( ). Three classes of chimeras were generated by the crossover events indicated by the lines. Class I chimeras exhibit specificity, class II chimeras exhibit and specificity, and class III chimeras have switched from to specificity ( ). N2 and C2 refer to the borders of the specificity region; N1 and C1 refer to the borders of the specificity region. The class II chimeras have N1 C2 borders, that is, they share one border with and the other with . Because class II chimeras have both and specificity, it has been proposed that differences at only one border are sufficient for dimerization and generation of the active heterodimer ( ). The specificity region for encompasses a region of approximately 40 amino acids, and that of encompasses a region of approximately 70 amino acids ( ). Similar conclusions were reached by Kämper et al. ( ) from yeast two-hybrid interactions and analysis of alleles.
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Figure 21.7

chimeric alleles delimit the specificity region. Chimeras between and or between and were generated by homologous recombination at the locus ( ). Three classes of chimeras were generated by the crossover events indicated by the lines. Class I chimeras exhibit specificity, class II chimeras exhibit and specificity, and class III chimeras have switched from to specificity ( ). N2 and C2 refer to the borders of the specificity region; N1 and C1 refer to the borders of the specificity region. The class II chimeras have N1 C2 borders, that is, they share one border with and the other with . Because class II chimeras have both and specificity, it has been proposed that differences at only one border are sufficient for dimerization and generation of the active heterodimer ( ). The specificity region for encompasses a region of approximately 40 amino acids, and that of encompasses a region of approximately 70 amino acids ( ). Similar conclusions were reached by Kämper et al. ( ) from yeast two-hybrid interactions and analysis of alleles.

Citation: Banuett F. 2007. History of the Mating Types in , p 351-375. In Heitman J, Kronstad J, Taylor J, Casselton L (ed), Sex in Fungi. ASM Press, Washington, DC. doi: 10.1128/9781555815837.ch21
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Figure 21.8
Molecular structure and organization of the locus. The locus has two alleles, and ( ), and codes for components of a pheromone response pathway ( ). Both and contain a pheromone precursor and a receptor gene. The pheromone precursor genes code for polypeptides of 40 and 38 amino acids for and , respectively, and the pheromone precursors contain a CAAX box at the C terminus ( ). This sequence is a substrate for prenylation and carboxymethylation, and the modification is necessary for full activity of the mature pheromones ( ). The modified pheromone precursors are processed further to yield lipopeptides of 13 and 9 amino acids for and , respectively. The allele contains additional genes: and , and a pseudopheromone gene, ( ), not present in the allele. (From reference with permission.)
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Image of Figure 21.8
Figure 21.8

Molecular structure and organization of the locus. The locus has two alleles, and ( ), and codes for components of a pheromone response pathway ( ). Both and contain a pheromone precursor and a receptor gene. The pheromone precursor genes code for polypeptides of 40 and 38 amino acids for and , respectively, and the pheromone precursors contain a CAAX box at the C terminus ( ). This sequence is a substrate for prenylation and carboxymethylation, and the modification is necessary for full activity of the mature pheromones ( ). The modified pheromone precursors are processed further to yield lipopeptides of 13 and 9 amino acids for and , respectively. The allele contains additional genes: and , and a pseudopheromone gene, ( ), not present in the allele. (From reference with permission.)

Citation: Banuett F. 2007. History of the Mating Types in , p 351-375. In Heitman J, Kronstad J, Taylor J, Casselton L (ed), Sex in Fungi. ASM Press, Washington, DC. doi: 10.1128/9781555815837.ch21
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References

/content/book/10.1128/9781555815837.ch21
1. Abe, K.,, I. Kusaka, and, S. Fukui. 1975. Morphological change in the early stages of the mating process of Rhodosporidium toruloides. J. Bacteriol. 122: 710– 718.
2. Agrios, G. N. 1994. Plant Pathology, 4th ed. Academic Press, New York, NY.
3. Akada, R.,, K. Minomi,, J. Kai,, I. Yamashita,, T. Miyakawa, and, S. Fukui. 1989. Multiple genes coding for precursors of rhodotorucine A, a farnesyl peptide mating pheromone of the basidiomycetous yeast Rhodosporidium toruloides. Mol. Cell. Biol. 9: 3491– 3498.
4. Alexopoulos, C. J.,, C. W. Mims, and, M. Blackwell. 1996. Introductory Mycology, 4th ed. Wiley, Hoboken, NJ.
5. Bakkeren, G.,, G. Jiang,, R. L. Warren,, Y. Butterfield,, H. Shin,, R. Chiu,, R. Linning,, J. Schein,, N. Lee,, G. Hu,, D. M. Kupfer,, Y. Tang,, B. A. Roe,, S. Jones,, M. Marra, and, J. W. Kronstad. 2006. Mating factor linkage and genome evolution in basidiomycetous pathogens of cereals. Fungal Genet. Biol. 43: 655– 666.
6. Bakkeren, G., and, J. W. Kronstad. 1994. Linkage of mating-type loci distinguishes bipolar from tetrapolar mating in basidiomycetous smut fungi. Proc. Natl. Acad. Sci. USA 91: 7085– 7089.
7. Banham, A. H.,, R. N. Asante-Owusu,, B. Göttgens, S. Thompson,, C. S. Kingsnorth,, E. Mellor, and, L. A. Casselton. 1995. An N-terminal dimerization domain permits homeodomain proteins to choose compatible partners and initiate sexual development in the mushroom Coprinus cinereus. Plant Cell 7: 773– 783.
8. Banuett, F. 2002. Pathogenic development in Ustilago maydis: a progression of morphological transitions that results in tumor formation and teliospore production, p. 349–398. In H. D. Osiewacz (ed.), Molecular Biology of Fungal Development. Marcel Dekker, New York, NY.
9. Banuett, F. 1998. Signalling in the yeasts: an informational cascade with links to the filamentous fungi. Microbiol. Mol. Biol. Rev. 62: 249– 274.
10. Banuett,, F. 1995. Genetics of Ustilago maydis, a fungal pathogen that induces tumors in maize. Annu. Rev. Genet. 29: 179– 208.
11. Banuett, F. 1992. Ustilago maydis, the delightful blight. Trends Genet. 8: 17– 180.
12. Banuett, F. 1991. Identification of genes governing filamentous growth and tumor induction by the plant pathogen Ustilago maydis. Proc. Natl. Acad. Sci. USA 88: 3922– 3926.
13. Banuett,, F., and I. Herskowitz. 1996. Discrete developmental stages during teliospore formation in the corn smut fungus, Ustilago maydis. Development 122: 2965– 2976.
14. Banuett, F., and, I. Herskowitz. 1994. Identification of Fuz7, a Ustilago maydis MEK/MAPKK homolog required for a-locus-dependent and -independent steps in the fungal life cycle. Genes Dev. 8: 1367– 1378.
15. Banuett, F., and, I. Herskowitz. 1994. Morphological transitions in the life cycle of Ustilago maydis and their genetic control by the a and b loci. Exp. Mycol. 18: 247– 266.
16. Banuett, F., and, I. Herskowitz. 1989. Different a alleles of Ustilago maydis are necessary for maintenance of filamentous growth but not for meiosis. Proc. Natl. Acad. Sci. USA 86: 5878– 5882.
17. Banuett, F., and, I. Herskowitz. 1988. Ustilago maydis, smut of maize, p. 427–455. In G. Sidhu (ed.), Genetics of Plant Pathogenic Fungi. Advances in Plant Pathology, vol. 6. Academic Press, London, United Kingdom.
18. Barrett, K. J.,, S. E. Gold, and, J. W. Kronsttad. 1993. Identification and complementation of a mutation to constitutive filamentous growth in Ustilago maydis. Mol. Plant-Microbe Interact. 6: 274– 283.
19. Bauch, R. 1932. Die Sexualität von Ustilago scorzonerae und Ustilago zeae. Phytopathol. Zeit. 5: 315– 321.
20. Bauch,, R. 1923. Uber Ustilago longissima und ihre varietät macrospora. Zeit. Botan. 15: 241– 279
21. Bölker, M.,, M. Urban, and, R. Kahmann. 1992. The a mating type locus of U. maydis specifies cell signaling components. Cell 68: 441– 450.
22. Bortfeld, M.,, K. Auffarth,, R. Kahmann, and, C. W. Basse. 2004. The Ustilago maydis a2 mating-type locus genes lga2 and rga2 compromise pathogenicity in the absence of the mitochondrial p32 family protein Mrb1. Plant Cell 16: 2233– 2248.
23. Bowman, D. H. 1946. Sporidial fusion in Ustilago maydis. J. Agric. Res. 72: 233– 243.
24. Brefeld,, O. 1883. Botanische Untersuchungen über Hefenpilze. Fortsetzung der Schimmelpilze, p. 1–208. Untersuchungen aus dem Gesammtgebiete der Mykologie. Heft V. Die Brandpilze I (Ustilagineen). Verlag von Arthur Felix, Leipzig, Germany.
25. Bürglin, T. R. 1994. A comprehensive classification of homeobox genes, p. 27–71. In D. Deboule (ed.), Guidebook to the Homeobox Genes. Oxford University Press, Oxford, United Kingdom.
26. Christensen, J. J. 1963. Corn smut caused by Ustilago maydis. Am. Phytopathol. Soc. Monogr. No. 2.
27. Christensen,, J. J. 1931. Studies of the genetics of Ustilago zeae. Phytopathol. Zeit. 4: 129– 188.
28. Christensen, J. J. 1929. Mutation and hybridization in Ustilago zeae. Part II. Hybridization. Minn. Agric. Exp. Stn. Tech. Bull. 65: 89– 108.
29. Davey, J. 1992. Mating pheromones of the fission yeast Schizosaccharomyces pombe: purification and structural characterization of M-factor and isolation and analysis of two genes encoding the pheromone. EMBO J. 11: 951– 960.
30. Day, A. W., and, J. K. Jones. 1968. The production and characteristics of diploids in Ustilago violacea. Genet. Res. 11: 63– 81
31. Day, P. R., and, S. L. Anagnostakis. 1971. Corn smut dikaryon in culture. Nat. New Biol. 231: 19– 20.
32. Day, P. R.,, S. L. Anagnostakis, and, J. E. Puhalla. 1971. Pathogenicity resulting from mutation at the b locus of Ustilago maydis. Proc. Natl. Acad. Sci. USA 68: 533– 535.
33. Day, P. R. 1963. Mutations of the A mating type factor in Coprinus lagopus. Genet. Res. Camb. 4: 655– 664.
34. Day,, P. R. 1960. The structure of the A mating type locus in Coprinus lagopus. Genetics 45: 641– 650.
35. Dranginis, A. M. 1990. Binding of yeast a1 and alpha2 as a heterodimer to the operator DNA of a haploid-specific gene. Nature 347: 682– 685.
36. Feldbrügge,, M., J. Kämper, G. Steinberg, and, R. Kahmann. 2004. Regulation of mating and pathogenic development in Ustilago maydis. Curr. Opin. Microbiol. 7: 666– 672.
37. Fotheringham, S., and, W. K. Holloman. 1989. Cloning and disruption of Ustilago maydis genes. Mol. Cell. Biol. 9: 4052– 4055.
38. Froeliger, E. H., and, S. A. Leong. 1991. The a mating-type alleles of Ustilago maydis are idiomorphs. Gene 100: 113– 122.
39. Garcia-Muse, T.,, G. Steinberg, and, J. Perez-Martin. 2003. Pheromone-induced G2 arrest in the phytopathogenic fungus Ustilago maydis. Eukaryot. Cell 2: 494– 500.
40. Gillissen, B.,, J. Bergemann,, C. Sandmann,, B. Schroeer,, M. Bölker, and R. Kahmann. 1992. A two-component regulatory system for self/non-self recognition in Ustilago maydis. Cell 68: 647– 657.
41. Goutte, C., and, A. D. Johnson. 1994. Recognition of a DNA operator by a dimer composed of two different homeodomain proteins. EMBO J. 13: 1434– 1442.
42. Goutte, C., and, A. D. Johnson. 1993. Yeast a1 and alpha2 homeodomain proteins form a DNA-binding activity with properties distinct from those of either protein. J. Mol. Biol. 233: 359– 371.
43. Hanna, W. F. 1929. Studies in the physiology and cytology of Ustilago zeae and Sorosporium reilianum. Phytopathology 19: 415– 441.
44. Hanna,, W. F. 1925. The problem of sex in Coprinus lagopus. Ann. Bot. 39: 431– 457.
45. Hartmann, H. A.,, R. Kahmann, and, M. Bölker. 1996. The pheromone response factor coordinates filamentous growth and pathogenicity in Ustilago maydis. EMBO J. 15: 1632– 1641.
46. Herskowitz, I. 1989. A regulatory hierarchy for cell specialization in yeast. Nature 342: 749– 757.
47. Herskowitz, I. 1988. Life cycle of the budding yeast Saccharomyces cerevisiae. Microbiol. Rev. 52: 536– 553.
48. Holliday, R. 1974. Ustilago maydis, p. 575–595. In R. C. King (ed.), Handbook of Genetics, vol 1. Plenum, New York, NY.
49. Holliday, R. 1961. The genetics of Ustilago maydis. Genet. Res. 2: 204– 230.
50. Holliday,, R. 1961. Induced mitotic crossing-over in Ustilago maydis. Genet. Res. 2: 231– 248.
51. Kahmann, R.,, T. Romeis,, M. Bölker, and J. Kämper. 1995. Control of mating and development in Ustilago maydis. Curr. Opin. Genet. Dev. 5: 559– 564.
52. Kahmann, R., and, C. Basse. 2001. Fungal gene expression during pathogenesis-related development and host plant colonization. Curr. Opin. Microbiol. 4: 374– 380.
53. Kahmann, R., and, M. Bölker. 1996. Self/nonself recognition in fungi: old mysteries and simple solutions. Cell 85: 145– 148.
54. Kämper, J.,, M. Reichmann,, T. Romeis,, M. Bölker, and R. Kahmann. 1995. Multiallelic recognition: nonself-dependent dimerization of the bE and bW homeodomain proteins in Ustilago maydis. Cell 81: 73– 83.
55. Kniep, H. 1919. Untersuchungen über den Antheren-brand ( Ustilago violacea Pers.). Ein Beitrag zum Sexual-itätsproblem. Zeit. Bot. 11: 257– 284.
56. Kronstad,, J. W., and S. A. Leong. 1990. The b mating-type locus of Ustilago maydis contains variable and constant regions. Genes Dev. 4: 1384– 1395.
57. Kronstad, J. W., and, S. A. Leong. 1989. Isolation of two alleles of the b locus of Ustilago maydis. Proc. Natl. Acad. Sci. USA 86: 978– 982.
58. Kronstad, J. W.,, J. Wang,, S. F. Covert,, D. W. Holden,, G. S. McKnight, and S. A. Leong. 1989. Isolation of metabolic genes and demonstration of gene disruption in the phytopathogenic fungus Ustilago maydis. Gene 79: 97– 106.
59. Kües, U.,, R. N. Asante-Owusu,, E. S. Mutasa,, A. M. Tymon,, E. H. Pardo,, S. F. O’Shea,, B. Göttgens, and L. A. Casselton. 1994. Two classes of homeodomain proteins specify multiple A mating types of the mushroom Coprinus cinereus. Plant Cell 6: 1467– 1475.
60. Kües, U.,, B. Göttgens, R. Stratmann,, W. V. Richardson,, S. F. O’Shea, and L. A. Casselton. 1994. A chimeric homeodomain protein causes self-compatibility and constitutive sexual development in the mushroom Coprinus cinereus. EMBO J. 13: 4054– 4059.
61. Kües, U.,, W. V. Richardson,, A. M. Tymon,, E. S. Mutasa,, B. Göttgens, S. Gaubatz,, A. Gregoriades, and, L. A. Casselton. 1992. The combination of dissimilar alleles of the A alpha and A beta gene complexes, whose proteins contain homeodomain motifs determines sexual development in the mushroom Coprinus cinereus. Genes Dev. 6: 568– 577.
62. Kuhn, J., and, Y. Parag. 1972. Protein-subunit aggregation model for self-incompatibility in higher fungi. J. Theor. Biol. 35: 77– 91.
63. Laity, C.,, L. Giasson,, R. Campbell, and, J. Kronstad. 1995. Heterozygosity at the b mating-type locus attenuates fusion in Ustilago maydis. Curr. Genet. 27: 451– 459.
64. Lederberg, J., and, W. M. Lederberg. 1952. Replica plating and indirect selection of bacterial mutants. J. Bacteriol. 63: 399– 406.
65. Lengeler, K. B.,, D. S. Fox,, J. A. Fraser,, A. Allen,, K. Forrester,, F. S. Dietrich, and, J. Heitman. 2002. Mating-type locus of Cryptococcus neoformans: a step in the evolution of sex chromosomes. Eukaryot. Cell 5: 704– 718.
66. Luo, Y.,, R. C. Ullrich, and, C. P. Novotny. 1994. Only one of the paired Schizophyllum commune A alpha mating type, putative homeobox genes encodes a homeodomain essential for A alpha-regulated development. Mol. Gen. Genet. 244: 318– 324.
67. Martínez-Espinoza, A. D.,, S. A. Gerhardt, and, J. W. Sherwood. 1993. Morphological and mutational analysis of mating in Ustilago hordei. Exp. Mycol. 17: 200– 214.
68. O’Donnell, K. L, and, K. J. McLaughlin. 1984. Postmeiotic mitosis, basidiospore development and septation in Ustilago maydis. Mycologia 76: 486– 502.
69. Perkins, D. D. 1949. Biochemical mutants in the smut fungus Ustilago maydis. Genetics 34: 607– 626.
70. Puhalla,, J. E. 1970. Genetic studies of the b incompatibility locus of Ustilago maydis. Genet. Res. 16: 229– 232.
71. Puhalla, J. E. 1968. Compatibility reactions on solid medium and interstrain inhibition in Ustilago maydis. Genetics 60: 461– 474.
72. Raper,, J. R., M. G. Baxter, and, A. H. Ellingboe. 1960. The genetic structure of the incompatibility factors of Schizophyllum commune: the A factor. Proc. Natl. Acad. Sci. USA 46: 833– 842.
73. Robertson, C. I.,, K. A. McMahon,, K. Toenjes,, C. P. Novotny, and, R. C. Ullrich. 2002. Evidence for interaction of Schizophyllum commune Y mating-type proteins in vivo. Genetics 160: 1461– 1467.
74. Romeis, T.,, A. Brachmann,, R. Kahmann, and, J. Kämper. 2000. Identification of a target gene for the bE-bW homeodomain protein complex in Ustilago maydis. Mol. Microbiol. 37: 54– 66.
75. Romeis, T.,, J. Kämper, and R. Kahmann. 1997. Single-chain fusions of two unrelated homeodomain proteins trigger pathogenicity in Ustilago maydis. Proc. Natl. Acad. Sci. USA 94: 1230– 1234.
76. Rowell, J. B. 1955. Functional role of compatibility factors: an in vitro test for sexual compatibility with haploid lines of Ustilago zeae. Phytopathology 45: 370– 374.
77. Rowell,, J. B. 1955. Segregation of sex factors in a diploid line of Ustilago zeae induced by alpha radiation. Science 121: 304– 306.
78. Rowell, J. B., and, J. E. DeVay. 1954. Genetics of Ustilago zeae in relation to basic problems of its pathogenicity. Phytopathology 44: 356– 362.
79. Schafer, W. R., and, J. Rine. 1992. Protein prenylation: genes, enzymes, targets, and functions. Annu. Rev. Genet. 26: 209– 237.
80. Schirawski, J.,, B. Heinze,, M. Wagenknecht, and, R. Kahmann. 2005. Mating type loci of Sporisorium reilianum: novel pattern with three a and multiple b specificities. Eukaryot. Cell 4: 1317– 1327.
81. Schlesinger, R.,, R. Kahmann, and, J. Kämper. 1997. The homeodomains of the heterodimeric bE and bW proteins of Ustilago maydis are both critical for function. Mol. Gen. Genet. 254: 514– 519.
82. Schulz, B.,, F. Banuett,, M. Dahl,, R. Schlesinger,, W. Schäfer, T. Martin,, I. Herskowitz, and, R. Kahmann. 1990. The b alleles of U. maydis, whose combinations program pathogenic development, code for polypeptides containing a homeodomain-related motif. Cell 60: 295– 306.
83. Sleumer, H. O. 1932. Uber Sexualität und Zytologie von Ustilago zeae (Beckm.) Unger. Zeit. Bot. 25: 209– 263.
84. Snetselaar,, K. M. 1993. Microscopic observation of Ustilago maydis mating interactions. Exp. Mycol. 17: 345– 355.
85. Snetselaar, K. M.,, M. Bölker, and R. Kahmann. 1996. Ustilago maydis mating hyphae orient their growth toward pheromone sources. Fungal Genet. Biol. 20: 299– 312.
86. Spellig, T.,, M. Bölker, F. Lottspeich,, R. W. Frank, and, R. Kahmann. 1994. Pheromones trigger filamentous growth in Ustilago maydis. EMBO J. 13: 1620– 1627.
87. Stakman, E. C., and, J. J. Christensen. 1927. Heterothallism in Ustilago zeae. Phytopathology 17: 827– 834.
88. Stankis, M. M.,, C. A. Specht,, H. Yang,, L. Giasson,, R. C. Ullrich, and, C. P. Novotny. 1992. The A alpha mating locus of Schizophyllum commune encodes two dissimilar multiallelic homeodomain proteins. Proc. Natl. Acad. Sci. USA 89: 7169– 7173.
89. Ullrich, R. C. 1978. On the regulation of gene expression: incompatibility in Schizophyllum. Genetics 88: 709– 722.
90. Urban,, M., R. Kahmann, and, M. Bölker. 1996. Identification of the pheromone response element in Ustilago maydis. Mol. Gen. Genet. 251: 31– 37.
91. Urban, M.,, R. Kahmann, and, M. Bölker. 1996. The biallelic a mating type locus of Ustilago maydis:remnants of an additional pheromone gene indicate evolution from a multiallelic ancestor. Mol. Gen. Genet. 250: 414– 420.
92. Vershon, A. K.,, Y. S. Yin, and, A. D. Johnson. 1995. A homeodomain protein lacking specific side chains of helix 3 can still bind DNA and direct transcriptional repression. Genes Dev. 9: 182– 192.
93. Wang, J.,, D. W. Holden, and, S. A. Leong. 1988. Gene transfer system for the phytopathogenic fungus Ustilago maydis. Proc. Natl. Acad. Sci. USA 85: 865– 869.
94. Wong, G. J., and, K. Wells. 1985. Modified bifactorial incompatibility in Tremella mesenterica. Trans. Br. Mycol. Soc. 84: 834– 838.
95. Wu, J.,, R. C. Ullrich, and, C. P. Novotny. 1996. Regions in the Z5 mating type gene of Schizophyllum commune involved in Y-Z binding recognition. Mol. Gen. Genet. 252: 739– 745.
96. Yee, A. R., and, J. W. Kronstad. 1998. Dual sets of chimeric alleles identify specificity sequences for the bE and bW mating and pathogenicity genes of Ustilago maydis. Mol. Cell. Biol. 18: 221– 232.
97. Yee, A. R., and, J. W. Kronstad. 1993. Construction of chimeric alleles with altered specificity at the b incompatibility locus of Ustilago maydis. Proc. Natl. Acad. Sci. USA 90: 664– 668.
98. Yue, C.,, M. Osier,, C. P. Novotny, and, R. C. Ullrich. 1997. The specificity determinant of the Y mating-type proteins of Schizophyllum commune is also essential for Y-Z protein binding. Genetics 145: 253– 260.
99. Zhang, F. L., and, P. J. Casey. 1996. Protein prenylation: molecular mechanisms and functional consequences. Annu. Rev. Biochem. 65: 241– 269.

Tables

History of the Mating Types in Ustilago maydis
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Citation: Banuett F. 2007. History of the Mating Types in , p 351-375. In Heitman J, Kronstad J, Taylor J, Casselton L (ed), Sex in Fungi. ASM Press, Washington, DC. doi: 10.1128/9781555815837.ch21
/content/10.1128/9781555815837.ch21.ch21tab01
Table 21.1
The locus is multiallelic
Generic image for table
Table 21.1

The locus is multiallelic

Citation: Banuett F. 2007. History of the Mating Types in , p 351-375. In Heitman J, Kronstad J, Taylor J, Casselton L (ed), Sex in Fungi. ASM Press, Washington, DC. doi: 10.1128/9781555815837.ch21
/content/10.1128/9781555815837.ch21.ch21tab02
Table 21.2
Compatibility reactions among progeny from cross 10A4 × 17D4 and from solopathogen 410qq
Generic image for table
Table 21.2

Compatibility reactions among progeny from cross 10A4 × 17D4 and from solopathogen 410qq

Citation: Banuett F. 2007. History of the Mating Types in , p 351-375. In Heitman J, Kronstad J, Taylor J, Casselton L (ed), Sex in Fungi. ASM Press, Washington, DC. doi: 10.1128/9781555815837.ch21

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