Morphology transition genes in the dimorphic fission yeast Schizosaccharomycesjaponicus
Abstract The ability of the saprophytic fungus Schizosaccharomyces japonicus to alternate between unicellular yeast form and multicellular true mycelium makes this organism an attractive non-pathogenic model for the investigation of di- and polymorphism critical for pathogenicity in many pathogenic...
Ausführliche Beschreibung
Autor*in: |
Enczi, Klara [verfasserIn] Yamaguchi, Masashi [verfasserIn] Sipiczki, Matthias [verfasserIn] |
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Format: |
E-Artikel |
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Sprache: |
Englisch |
Erschienen: |
2007 |
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Schlagwörter: |
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Übergeordnetes Werk: |
Enthalten in: Antonie van Leeuwenhoek - Dordrecht [u.a.] : Springer Science + Business Media B.V, 1934, 92(2007), 2 vom: 14. Feb., Seite 143-154 |
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Übergeordnetes Werk: |
volume:92 ; year:2007 ; number:2 ; day:14 ; month:02 ; pages:143-154 |
Links: |
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DOI / URN: |
10.1007/s10482-007-9142-x |
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Katalog-ID: |
SPR010364919 |
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520 | |a Abstract The ability of the saprophytic fungus Schizosaccharomyces japonicus to alternate between unicellular yeast form and multicellular true mycelium makes this organism an attractive non-pathogenic model for the investigation of di- and polymorphism critical for pathogenicity in many pathogenic fungi. In a previous work we described three mutations that made the cells unable to form hyphae. Here we report on the isolation of additional mycelium-minus mutants and show that the mutations represent seven genes. Apart from the inhibition of the yeast-to-mycelium transition, the mutations also cause drastic changes in the yeast phase. Cells of myc3-34 and myc4-35 grow isotropically with apolar distribution of actin and randomised localisation of division planes. The mutants myc1-4, myc1-10, myc1-36, myc5-39 and myc6-43 form sep-like, branching microhyphae containing bipolarly growing cells. All mutants are defective in the polarisation of vacuole distribution, and myc3-34, myc4-35 and myc7-56 are also defective in vacuole fusion. The diversity of the mutant phenotypes indicates that several cellular processes must take place simultaneously for the transition from the yeast phase into the mycelial phase. | ||
650 | 4 | |a Fission yeast |7 (dpeaa)DE-He213 | |
650 | 4 | |a Dimorphism |7 (dpeaa)DE-He213 | |
650 | 4 | |a Morphogenesis |7 (dpeaa)DE-He213 | |
650 | 4 | |a Cell polarity |7 (dpeaa)DE-He213 | |
650 | 4 | |a Septum |7 (dpeaa)DE-He213 | |
650 | 4 | |a Vacuole |7 (dpeaa)DE-He213 | |
700 | 1 | |a Yamaguchi, Masashi |e verfasserin |4 aut | |
700 | 1 | |a Sipiczki, Matthias |e verfasserin |4 aut | |
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allfields |
10.1007/s10482-007-9142-x doi (DE-627)SPR010364919 (SPR)s10482-007-9142-x-e DE-627 ger DE-627 rakwb eng 570 610 ASE 42.30 bkl Enczi, Klara verfasserin aut Morphology transition genes in the dimorphic fission yeast Schizosaccharomycesjaponicus 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract The ability of the saprophytic fungus Schizosaccharomyces japonicus to alternate between unicellular yeast form and multicellular true mycelium makes this organism an attractive non-pathogenic model for the investigation of di- and polymorphism critical for pathogenicity in many pathogenic fungi. In a previous work we described three mutations that made the cells unable to form hyphae. Here we report on the isolation of additional mycelium-minus mutants and show that the mutations represent seven genes. Apart from the inhibition of the yeast-to-mycelium transition, the mutations also cause drastic changes in the yeast phase. Cells of myc3-34 and myc4-35 grow isotropically with apolar distribution of actin and randomised localisation of division planes. The mutants myc1-4, myc1-10, myc1-36, myc5-39 and myc6-43 form sep-like, branching microhyphae containing bipolarly growing cells. All mutants are defective in the polarisation of vacuole distribution, and myc3-34, myc4-35 and myc7-56 are also defective in vacuole fusion. The diversity of the mutant phenotypes indicates that several cellular processes must take place simultaneously for the transition from the yeast phase into the mycelial phase. Fission yeast (dpeaa)DE-He213 Dimorphism (dpeaa)DE-He213 Morphogenesis (dpeaa)DE-He213 Cell polarity (dpeaa)DE-He213 Septum (dpeaa)DE-He213 Vacuole (dpeaa)DE-He213 Yamaguchi, Masashi verfasserin aut Sipiczki, Matthias verfasserin aut Enthalten in Antonie van Leeuwenhoek Dordrecht [u.a.] : Springer Science + Business Media B.V, 1934 92(2007), 2 vom: 14. Feb., Seite 143-154 (DE-627)270929355 (DE-600)1478112-8 1572-9699 nnns volume:92 year:2007 number:2 day:14 month:02 pages:143-154 https://dx.doi.org/10.1007/s10482-007-9142-x lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_381 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 42.30 ASE AR 92 2007 2 14 02 143-154 |
spelling |
10.1007/s10482-007-9142-x doi (DE-627)SPR010364919 (SPR)s10482-007-9142-x-e DE-627 ger DE-627 rakwb eng 570 610 ASE 42.30 bkl Enczi, Klara verfasserin aut Morphology transition genes in the dimorphic fission yeast Schizosaccharomycesjaponicus 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract The ability of the saprophytic fungus Schizosaccharomyces japonicus to alternate between unicellular yeast form and multicellular true mycelium makes this organism an attractive non-pathogenic model for the investigation of di- and polymorphism critical for pathogenicity in many pathogenic fungi. In a previous work we described three mutations that made the cells unable to form hyphae. Here we report on the isolation of additional mycelium-minus mutants and show that the mutations represent seven genes. Apart from the inhibition of the yeast-to-mycelium transition, the mutations also cause drastic changes in the yeast phase. Cells of myc3-34 and myc4-35 grow isotropically with apolar distribution of actin and randomised localisation of division planes. The mutants myc1-4, myc1-10, myc1-36, myc5-39 and myc6-43 form sep-like, branching microhyphae containing bipolarly growing cells. All mutants are defective in the polarisation of vacuole distribution, and myc3-34, myc4-35 and myc7-56 are also defective in vacuole fusion. The diversity of the mutant phenotypes indicates that several cellular processes must take place simultaneously for the transition from the yeast phase into the mycelial phase. Fission yeast (dpeaa)DE-He213 Dimorphism (dpeaa)DE-He213 Morphogenesis (dpeaa)DE-He213 Cell polarity (dpeaa)DE-He213 Septum (dpeaa)DE-He213 Vacuole (dpeaa)DE-He213 Yamaguchi, Masashi verfasserin aut Sipiczki, Matthias verfasserin aut Enthalten in Antonie van Leeuwenhoek Dordrecht [u.a.] : Springer Science + Business Media B.V, 1934 92(2007), 2 vom: 14. Feb., Seite 143-154 (DE-627)270929355 (DE-600)1478112-8 1572-9699 nnns volume:92 year:2007 number:2 day:14 month:02 pages:143-154 https://dx.doi.org/10.1007/s10482-007-9142-x lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_381 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 42.30 ASE AR 92 2007 2 14 02 143-154 |
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10.1007/s10482-007-9142-x doi (DE-627)SPR010364919 (SPR)s10482-007-9142-x-e DE-627 ger DE-627 rakwb eng 570 610 ASE 42.30 bkl Enczi, Klara verfasserin aut Morphology transition genes in the dimorphic fission yeast Schizosaccharomycesjaponicus 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract The ability of the saprophytic fungus Schizosaccharomyces japonicus to alternate between unicellular yeast form and multicellular true mycelium makes this organism an attractive non-pathogenic model for the investigation of di- and polymorphism critical for pathogenicity in many pathogenic fungi. In a previous work we described three mutations that made the cells unable to form hyphae. Here we report on the isolation of additional mycelium-minus mutants and show that the mutations represent seven genes. Apart from the inhibition of the yeast-to-mycelium transition, the mutations also cause drastic changes in the yeast phase. Cells of myc3-34 and myc4-35 grow isotropically with apolar distribution of actin and randomised localisation of division planes. The mutants myc1-4, myc1-10, myc1-36, myc5-39 and myc6-43 form sep-like, branching microhyphae containing bipolarly growing cells. All mutants are defective in the polarisation of vacuole distribution, and myc3-34, myc4-35 and myc7-56 are also defective in vacuole fusion. The diversity of the mutant phenotypes indicates that several cellular processes must take place simultaneously for the transition from the yeast phase into the mycelial phase. Fission yeast (dpeaa)DE-He213 Dimorphism (dpeaa)DE-He213 Morphogenesis (dpeaa)DE-He213 Cell polarity (dpeaa)DE-He213 Septum (dpeaa)DE-He213 Vacuole (dpeaa)DE-He213 Yamaguchi, Masashi verfasserin aut Sipiczki, Matthias verfasserin aut Enthalten in Antonie van Leeuwenhoek Dordrecht [u.a.] : Springer Science + Business Media B.V, 1934 92(2007), 2 vom: 14. Feb., Seite 143-154 (DE-627)270929355 (DE-600)1478112-8 1572-9699 nnns volume:92 year:2007 number:2 day:14 month:02 pages:143-154 https://dx.doi.org/10.1007/s10482-007-9142-x lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_381 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 42.30 ASE AR 92 2007 2 14 02 143-154 |
allfieldsGer |
10.1007/s10482-007-9142-x doi (DE-627)SPR010364919 (SPR)s10482-007-9142-x-e DE-627 ger DE-627 rakwb eng 570 610 ASE 42.30 bkl Enczi, Klara verfasserin aut Morphology transition genes in the dimorphic fission yeast Schizosaccharomycesjaponicus 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract The ability of the saprophytic fungus Schizosaccharomyces japonicus to alternate between unicellular yeast form and multicellular true mycelium makes this organism an attractive non-pathogenic model for the investigation of di- and polymorphism critical for pathogenicity in many pathogenic fungi. In a previous work we described three mutations that made the cells unable to form hyphae. Here we report on the isolation of additional mycelium-minus mutants and show that the mutations represent seven genes. Apart from the inhibition of the yeast-to-mycelium transition, the mutations also cause drastic changes in the yeast phase. Cells of myc3-34 and myc4-35 grow isotropically with apolar distribution of actin and randomised localisation of division planes. The mutants myc1-4, myc1-10, myc1-36, myc5-39 and myc6-43 form sep-like, branching microhyphae containing bipolarly growing cells. All mutants are defective in the polarisation of vacuole distribution, and myc3-34, myc4-35 and myc7-56 are also defective in vacuole fusion. The diversity of the mutant phenotypes indicates that several cellular processes must take place simultaneously for the transition from the yeast phase into the mycelial phase. Fission yeast (dpeaa)DE-He213 Dimorphism (dpeaa)DE-He213 Morphogenesis (dpeaa)DE-He213 Cell polarity (dpeaa)DE-He213 Septum (dpeaa)DE-He213 Vacuole (dpeaa)DE-He213 Yamaguchi, Masashi verfasserin aut Sipiczki, Matthias verfasserin aut Enthalten in Antonie van Leeuwenhoek Dordrecht [u.a.] : Springer Science + Business Media B.V, 1934 92(2007), 2 vom: 14. Feb., Seite 143-154 (DE-627)270929355 (DE-600)1478112-8 1572-9699 nnns volume:92 year:2007 number:2 day:14 month:02 pages:143-154 https://dx.doi.org/10.1007/s10482-007-9142-x lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_381 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 42.30 ASE AR 92 2007 2 14 02 143-154 |
allfieldsSound |
10.1007/s10482-007-9142-x doi (DE-627)SPR010364919 (SPR)s10482-007-9142-x-e DE-627 ger DE-627 rakwb eng 570 610 ASE 42.30 bkl Enczi, Klara verfasserin aut Morphology transition genes in the dimorphic fission yeast Schizosaccharomycesjaponicus 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract The ability of the saprophytic fungus Schizosaccharomyces japonicus to alternate between unicellular yeast form and multicellular true mycelium makes this organism an attractive non-pathogenic model for the investigation of di- and polymorphism critical for pathogenicity in many pathogenic fungi. In a previous work we described three mutations that made the cells unable to form hyphae. Here we report on the isolation of additional mycelium-minus mutants and show that the mutations represent seven genes. Apart from the inhibition of the yeast-to-mycelium transition, the mutations also cause drastic changes in the yeast phase. Cells of myc3-34 and myc4-35 grow isotropically with apolar distribution of actin and randomised localisation of division planes. The mutants myc1-4, myc1-10, myc1-36, myc5-39 and myc6-43 form sep-like, branching microhyphae containing bipolarly growing cells. All mutants are defective in the polarisation of vacuole distribution, and myc3-34, myc4-35 and myc7-56 are also defective in vacuole fusion. The diversity of the mutant phenotypes indicates that several cellular processes must take place simultaneously for the transition from the yeast phase into the mycelial phase. Fission yeast (dpeaa)DE-He213 Dimorphism (dpeaa)DE-He213 Morphogenesis (dpeaa)DE-He213 Cell polarity (dpeaa)DE-He213 Septum (dpeaa)DE-He213 Vacuole (dpeaa)DE-He213 Yamaguchi, Masashi verfasserin aut Sipiczki, Matthias verfasserin aut Enthalten in Antonie van Leeuwenhoek Dordrecht [u.a.] : Springer Science + Business Media B.V, 1934 92(2007), 2 vom: 14. Feb., Seite 143-154 (DE-627)270929355 (DE-600)1478112-8 1572-9699 nnns volume:92 year:2007 number:2 day:14 month:02 pages:143-154 https://dx.doi.org/10.1007/s10482-007-9142-x lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_381 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 42.30 ASE AR 92 2007 2 14 02 143-154 |
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Enthalten in Antonie van Leeuwenhoek 92(2007), 2 vom: 14. Feb., Seite 143-154 volume:92 year:2007 number:2 day:14 month:02 pages:143-154 |
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Enczi, Klara @@aut@@ Yamaguchi, Masashi @@aut@@ Sipiczki, Matthias @@aut@@ |
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In a previous work we described three mutations that made the cells unable to form hyphae. Here we report on the isolation of additional mycelium-minus mutants and show that the mutations represent seven genes. Apart from the inhibition of the yeast-to-mycelium transition, the mutations also cause drastic changes in the yeast phase. Cells of myc3-34 and myc4-35 grow isotropically with apolar distribution of actin and randomised localisation of division planes. The mutants myc1-4, myc1-10, myc1-36, myc5-39 and myc6-43 form sep-like, branching microhyphae containing bipolarly growing cells. All mutants are defective in the polarisation of vacuole distribution, and myc3-34, myc4-35 and myc7-56 are also defective in vacuole fusion. 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Enczi, Klara |
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Enczi, Klara ddc 570 bkl 42.30 misc Fission yeast misc Dimorphism misc Morphogenesis misc Cell polarity misc Septum misc Vacuole Morphology transition genes in the dimorphic fission yeast Schizosaccharomycesjaponicus |
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570 610 ASE 42.30 bkl Morphology transition genes in the dimorphic fission yeast Schizosaccharomycesjaponicus Fission yeast (dpeaa)DE-He213 Dimorphism (dpeaa)DE-He213 Morphogenesis (dpeaa)DE-He213 Cell polarity (dpeaa)DE-He213 Septum (dpeaa)DE-He213 Vacuole (dpeaa)DE-He213 |
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morphology transition genes in the dimorphic fission yeast schizosaccharomycesjaponicus |
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Morphology transition genes in the dimorphic fission yeast Schizosaccharomycesjaponicus |
abstract |
Abstract The ability of the saprophytic fungus Schizosaccharomyces japonicus to alternate between unicellular yeast form and multicellular true mycelium makes this organism an attractive non-pathogenic model for the investigation of di- and polymorphism critical for pathogenicity in many pathogenic fungi. In a previous work we described three mutations that made the cells unable to form hyphae. Here we report on the isolation of additional mycelium-minus mutants and show that the mutations represent seven genes. Apart from the inhibition of the yeast-to-mycelium transition, the mutations also cause drastic changes in the yeast phase. Cells of myc3-34 and myc4-35 grow isotropically with apolar distribution of actin and randomised localisation of division planes. The mutants myc1-4, myc1-10, myc1-36, myc5-39 and myc6-43 form sep-like, branching microhyphae containing bipolarly growing cells. All mutants are defective in the polarisation of vacuole distribution, and myc3-34, myc4-35 and myc7-56 are also defective in vacuole fusion. The diversity of the mutant phenotypes indicates that several cellular processes must take place simultaneously for the transition from the yeast phase into the mycelial phase. |
abstractGer |
Abstract The ability of the saprophytic fungus Schizosaccharomyces japonicus to alternate between unicellular yeast form and multicellular true mycelium makes this organism an attractive non-pathogenic model for the investigation of di- and polymorphism critical for pathogenicity in many pathogenic fungi. In a previous work we described three mutations that made the cells unable to form hyphae. Here we report on the isolation of additional mycelium-minus mutants and show that the mutations represent seven genes. Apart from the inhibition of the yeast-to-mycelium transition, the mutations also cause drastic changes in the yeast phase. Cells of myc3-34 and myc4-35 grow isotropically with apolar distribution of actin and randomised localisation of division planes. The mutants myc1-4, myc1-10, myc1-36, myc5-39 and myc6-43 form sep-like, branching microhyphae containing bipolarly growing cells. All mutants are defective in the polarisation of vacuole distribution, and myc3-34, myc4-35 and myc7-56 are also defective in vacuole fusion. The diversity of the mutant phenotypes indicates that several cellular processes must take place simultaneously for the transition from the yeast phase into the mycelial phase. |
abstract_unstemmed |
Abstract The ability of the saprophytic fungus Schizosaccharomyces japonicus to alternate between unicellular yeast form and multicellular true mycelium makes this organism an attractive non-pathogenic model for the investigation of di- and polymorphism critical for pathogenicity in many pathogenic fungi. In a previous work we described three mutations that made the cells unable to form hyphae. Here we report on the isolation of additional mycelium-minus mutants and show that the mutations represent seven genes. Apart from the inhibition of the yeast-to-mycelium transition, the mutations also cause drastic changes in the yeast phase. Cells of myc3-34 and myc4-35 grow isotropically with apolar distribution of actin and randomised localisation of division planes. The mutants myc1-4, myc1-10, myc1-36, myc5-39 and myc6-43 form sep-like, branching microhyphae containing bipolarly growing cells. All mutants are defective in the polarisation of vacuole distribution, and myc3-34, myc4-35 and myc7-56 are also defective in vacuole fusion. The diversity of the mutant phenotypes indicates that several cellular processes must take place simultaneously for the transition from the yeast phase into the mycelial phase. |
collection_details |
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container_issue |
2 |
title_short |
Morphology transition genes in the dimorphic fission yeast Schizosaccharomycesjaponicus |
url |
https://dx.doi.org/10.1007/s10482-007-9142-x |
remote_bool |
true |
author2 |
Yamaguchi, Masashi Sipiczki, Matthias |
author2Str |
Yamaguchi, Masashi Sipiczki, Matthias |
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hochschulschrift_bool |
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doi_str |
10.1007/s10482-007-9142-x |
up_date |
2024-07-03T15:39:05.871Z |
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|
score |
7.400529 |