Kre29p is a novel nuclear protein involved in DNA repair and mitotic fidelity in Candida glabrata
Abstract Candida glabrata KRE29 is an ortholog of Saccharomyces cerevisiae KRE29. S. cerevisiae Kre29p has been identified by affinity purification as a subunit of the Smc5–Smc6 complex, which is required for DNA repair and chromosome segregation. However, mutant phenotypes of S. cerevisiae KRE29 ha...
Ausführliche Beschreibung
Autor*in: |
Miyazaki, Taiga [verfasserIn] |
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Format: |
E-Artikel |
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Sprache: |
Englisch |
Erschienen: |
2006 |
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Schlagwörter: |
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Anmerkung: |
© Springer-Verlag 2006 |
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Übergeordnetes Werk: |
Enthalten in: Current genetics - Berlin : Springer, 1979, 50(2006), 1 vom: 28. Apr., Seite 11-22 |
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Übergeordnetes Werk: |
volume:50 ; year:2006 ; number:1 ; day:28 ; month:04 ; pages:11-22 |
Links: |
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DOI / URN: |
10.1007/s00294-006-0072-3 |
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Katalog-ID: |
SPR003813525 |
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100 | 1 | |a Miyazaki, Taiga |e verfasserin |4 aut | |
245 | 1 | 0 | |a Kre29p is a novel nuclear protein involved in DNA repair and mitotic fidelity in Candida glabrata |
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520 | |a Abstract Candida glabrata KRE29 is an ortholog of Saccharomyces cerevisiae KRE29. S. cerevisiae Kre29p has been identified by affinity purification as a subunit of the Smc5–Smc6 complex, which is required for DNA repair and chromosome segregation. However, mutant phenotypes of S. cerevisiae KRE29 have not been well characterized and none of its orthologs’ functions has been reported. Here we report phenotypic characteristics of a C. glabratakre29 deletant. The absence of C. glabrata Kre29p resulted in decreased viability, exhibiting cell cycle arrest between late S-phase and metaphase even under normal growth conditions, and also caused an increase of plasmid loss rate, implying that Kre29p is required for mitotic chromosome transmission fidelity. The deletant showed increased sensitivity to high temperature as well as to DNA damaging agents including UV, gamma ray, 4-nitroquinoline-1-oxide and methyl methanesulfonate, and the phenotypes were restored in the KRE29 reintegrant. Consistent with the Δkre29 phenotypes, a Kre29p-GFP fusion protein was located in the nucleus. Furthermore, Kre29p-GFP became concentrated and formed distinct foci after exposure to 4-nitroquinoline-1-oxide. These results suggest the involvement of C. glabrata Kre29p in DNA repair. To our knowledge, this is the first report addressing a cellular protein involved in DNA repair in C. glabrata. | ||
650 | 4 | |a DNA damage |7 (dpeaa)DE-He213 | |
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650 | 4 | |a Nucleus |7 (dpeaa)DE-He213 | |
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700 | 1 | |a Tsai, Huei-Fung |4 aut | |
700 | 1 | |a Bennett, John E. |4 aut | |
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2006 |
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10.1007/s00294-006-0072-3 doi (DE-627)SPR003813525 (SPR)s00294-006-0072-3-e DE-627 ger DE-627 rakwb eng Miyazaki, Taiga verfasserin aut Kre29p is a novel nuclear protein involved in DNA repair and mitotic fidelity in Candida glabrata 2006 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer-Verlag 2006 Abstract Candida glabrata KRE29 is an ortholog of Saccharomyces cerevisiae KRE29. S. cerevisiae Kre29p has been identified by affinity purification as a subunit of the Smc5–Smc6 complex, which is required for DNA repair and chromosome segregation. However, mutant phenotypes of S. cerevisiae KRE29 have not been well characterized and none of its orthologs’ functions has been reported. Here we report phenotypic characteristics of a C. glabratakre29 deletant. The absence of C. glabrata Kre29p resulted in decreased viability, exhibiting cell cycle arrest between late S-phase and metaphase even under normal growth conditions, and also caused an increase of plasmid loss rate, implying that Kre29p is required for mitotic chromosome transmission fidelity. The deletant showed increased sensitivity to high temperature as well as to DNA damaging agents including UV, gamma ray, 4-nitroquinoline-1-oxide and methyl methanesulfonate, and the phenotypes were restored in the KRE29 reintegrant. Consistent with the Δkre29 phenotypes, a Kre29p-GFP fusion protein was located in the nucleus. Furthermore, Kre29p-GFP became concentrated and formed distinct foci after exposure to 4-nitroquinoline-1-oxide. These results suggest the involvement of C. glabrata Kre29p in DNA repair. To our knowledge, this is the first report addressing a cellular protein involved in DNA repair in C. glabrata. DNA damage (dpeaa)DE-He213 Cell cycle (dpeaa)DE-He213 Mitosis (dpeaa)DE-He213 Nucleus (dpeaa)DE-He213 Plasmid partitioning (dpeaa)DE-He213 Tsai, Huei-Fung aut Bennett, John E. aut Enthalten in Current genetics Berlin : Springer, 1979 50(2006), 1 vom: 28. Apr., Seite 11-22 (DE-627)253722136 (DE-600)1458984-9 1432-0983 nnns volume:50 year:2006 number:1 day:28 month:04 pages:11-22 https://dx.doi.org/10.1007/s00294-006-0072-3 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_152 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_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 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 AR 50 2006 1 28 04 11-22 |
spelling |
10.1007/s00294-006-0072-3 doi (DE-627)SPR003813525 (SPR)s00294-006-0072-3-e DE-627 ger DE-627 rakwb eng Miyazaki, Taiga verfasserin aut Kre29p is a novel nuclear protein involved in DNA repair and mitotic fidelity in Candida glabrata 2006 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer-Verlag 2006 Abstract Candida glabrata KRE29 is an ortholog of Saccharomyces cerevisiae KRE29. S. cerevisiae Kre29p has been identified by affinity purification as a subunit of the Smc5–Smc6 complex, which is required for DNA repair and chromosome segregation. However, mutant phenotypes of S. cerevisiae KRE29 have not been well characterized and none of its orthologs’ functions has been reported. Here we report phenotypic characteristics of a C. glabratakre29 deletant. The absence of C. glabrata Kre29p resulted in decreased viability, exhibiting cell cycle arrest between late S-phase and metaphase even under normal growth conditions, and also caused an increase of plasmid loss rate, implying that Kre29p is required for mitotic chromosome transmission fidelity. The deletant showed increased sensitivity to high temperature as well as to DNA damaging agents including UV, gamma ray, 4-nitroquinoline-1-oxide and methyl methanesulfonate, and the phenotypes were restored in the KRE29 reintegrant. Consistent with the Δkre29 phenotypes, a Kre29p-GFP fusion protein was located in the nucleus. Furthermore, Kre29p-GFP became concentrated and formed distinct foci after exposure to 4-nitroquinoline-1-oxide. These results suggest the involvement of C. glabrata Kre29p in DNA repair. To our knowledge, this is the first report addressing a cellular protein involved in DNA repair in C. glabrata. DNA damage (dpeaa)DE-He213 Cell cycle (dpeaa)DE-He213 Mitosis (dpeaa)DE-He213 Nucleus (dpeaa)DE-He213 Plasmid partitioning (dpeaa)DE-He213 Tsai, Huei-Fung aut Bennett, John E. aut Enthalten in Current genetics Berlin : Springer, 1979 50(2006), 1 vom: 28. Apr., Seite 11-22 (DE-627)253722136 (DE-600)1458984-9 1432-0983 nnns volume:50 year:2006 number:1 day:28 month:04 pages:11-22 https://dx.doi.org/10.1007/s00294-006-0072-3 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_152 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_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 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 AR 50 2006 1 28 04 11-22 |
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10.1007/s00294-006-0072-3 doi (DE-627)SPR003813525 (SPR)s00294-006-0072-3-e DE-627 ger DE-627 rakwb eng Miyazaki, Taiga verfasserin aut Kre29p is a novel nuclear protein involved in DNA repair and mitotic fidelity in Candida glabrata 2006 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer-Verlag 2006 Abstract Candida glabrata KRE29 is an ortholog of Saccharomyces cerevisiae KRE29. S. cerevisiae Kre29p has been identified by affinity purification as a subunit of the Smc5–Smc6 complex, which is required for DNA repair and chromosome segregation. However, mutant phenotypes of S. cerevisiae KRE29 have not been well characterized and none of its orthologs’ functions has been reported. Here we report phenotypic characteristics of a C. glabratakre29 deletant. The absence of C. glabrata Kre29p resulted in decreased viability, exhibiting cell cycle arrest between late S-phase and metaphase even under normal growth conditions, and also caused an increase of plasmid loss rate, implying that Kre29p is required for mitotic chromosome transmission fidelity. The deletant showed increased sensitivity to high temperature as well as to DNA damaging agents including UV, gamma ray, 4-nitroquinoline-1-oxide and methyl methanesulfonate, and the phenotypes were restored in the KRE29 reintegrant. Consistent with the Δkre29 phenotypes, a Kre29p-GFP fusion protein was located in the nucleus. Furthermore, Kre29p-GFP became concentrated and formed distinct foci after exposure to 4-nitroquinoline-1-oxide. These results suggest the involvement of C. glabrata Kre29p in DNA repair. To our knowledge, this is the first report addressing a cellular protein involved in DNA repair in C. glabrata. DNA damage (dpeaa)DE-He213 Cell cycle (dpeaa)DE-He213 Mitosis (dpeaa)DE-He213 Nucleus (dpeaa)DE-He213 Plasmid partitioning (dpeaa)DE-He213 Tsai, Huei-Fung aut Bennett, John E. aut Enthalten in Current genetics Berlin : Springer, 1979 50(2006), 1 vom: 28. Apr., Seite 11-22 (DE-627)253722136 (DE-600)1458984-9 1432-0983 nnns volume:50 year:2006 number:1 day:28 month:04 pages:11-22 https://dx.doi.org/10.1007/s00294-006-0072-3 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_152 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_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 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 AR 50 2006 1 28 04 11-22 |
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10.1007/s00294-006-0072-3 doi (DE-627)SPR003813525 (SPR)s00294-006-0072-3-e DE-627 ger DE-627 rakwb eng Miyazaki, Taiga verfasserin aut Kre29p is a novel nuclear protein involved in DNA repair and mitotic fidelity in Candida glabrata 2006 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer-Verlag 2006 Abstract Candida glabrata KRE29 is an ortholog of Saccharomyces cerevisiae KRE29. S. cerevisiae Kre29p has been identified by affinity purification as a subunit of the Smc5–Smc6 complex, which is required for DNA repair and chromosome segregation. However, mutant phenotypes of S. cerevisiae KRE29 have not been well characterized and none of its orthologs’ functions has been reported. Here we report phenotypic characteristics of a C. glabratakre29 deletant. The absence of C. glabrata Kre29p resulted in decreased viability, exhibiting cell cycle arrest between late S-phase and metaphase even under normal growth conditions, and also caused an increase of plasmid loss rate, implying that Kre29p is required for mitotic chromosome transmission fidelity. The deletant showed increased sensitivity to high temperature as well as to DNA damaging agents including UV, gamma ray, 4-nitroquinoline-1-oxide and methyl methanesulfonate, and the phenotypes were restored in the KRE29 reintegrant. Consistent with the Δkre29 phenotypes, a Kre29p-GFP fusion protein was located in the nucleus. Furthermore, Kre29p-GFP became concentrated and formed distinct foci after exposure to 4-nitroquinoline-1-oxide. These results suggest the involvement of C. glabrata Kre29p in DNA repair. To our knowledge, this is the first report addressing a cellular protein involved in DNA repair in C. glabrata. DNA damage (dpeaa)DE-He213 Cell cycle (dpeaa)DE-He213 Mitosis (dpeaa)DE-He213 Nucleus (dpeaa)DE-He213 Plasmid partitioning (dpeaa)DE-He213 Tsai, Huei-Fung aut Bennett, John E. aut Enthalten in Current genetics Berlin : Springer, 1979 50(2006), 1 vom: 28. Apr., Seite 11-22 (DE-627)253722136 (DE-600)1458984-9 1432-0983 nnns volume:50 year:2006 number:1 day:28 month:04 pages:11-22 https://dx.doi.org/10.1007/s00294-006-0072-3 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_152 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_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 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 AR 50 2006 1 28 04 11-22 |
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10.1007/s00294-006-0072-3 doi (DE-627)SPR003813525 (SPR)s00294-006-0072-3-e DE-627 ger DE-627 rakwb eng Miyazaki, Taiga verfasserin aut Kre29p is a novel nuclear protein involved in DNA repair and mitotic fidelity in Candida glabrata 2006 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer-Verlag 2006 Abstract Candida glabrata KRE29 is an ortholog of Saccharomyces cerevisiae KRE29. S. cerevisiae Kre29p has been identified by affinity purification as a subunit of the Smc5–Smc6 complex, which is required for DNA repair and chromosome segregation. However, mutant phenotypes of S. cerevisiae KRE29 have not been well characterized and none of its orthologs’ functions has been reported. Here we report phenotypic characteristics of a C. glabratakre29 deletant. The absence of C. glabrata Kre29p resulted in decreased viability, exhibiting cell cycle arrest between late S-phase and metaphase even under normal growth conditions, and also caused an increase of plasmid loss rate, implying that Kre29p is required for mitotic chromosome transmission fidelity. The deletant showed increased sensitivity to high temperature as well as to DNA damaging agents including UV, gamma ray, 4-nitroquinoline-1-oxide and methyl methanesulfonate, and the phenotypes were restored in the KRE29 reintegrant. Consistent with the Δkre29 phenotypes, a Kre29p-GFP fusion protein was located in the nucleus. Furthermore, Kre29p-GFP became concentrated and formed distinct foci after exposure to 4-nitroquinoline-1-oxide. These results suggest the involvement of C. glabrata Kre29p in DNA repair. To our knowledge, this is the first report addressing a cellular protein involved in DNA repair in C. glabrata. DNA damage (dpeaa)DE-He213 Cell cycle (dpeaa)DE-He213 Mitosis (dpeaa)DE-He213 Nucleus (dpeaa)DE-He213 Plasmid partitioning (dpeaa)DE-He213 Tsai, Huei-Fung aut Bennett, John E. aut Enthalten in Current genetics Berlin : Springer, 1979 50(2006), 1 vom: 28. Apr., Seite 11-22 (DE-627)253722136 (DE-600)1458984-9 1432-0983 nnns volume:50 year:2006 number:1 day:28 month:04 pages:11-22 https://dx.doi.org/10.1007/s00294-006-0072-3 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_152 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_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 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 AR 50 2006 1 28 04 11-22 |
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Enthalten in Current genetics 50(2006), 1 vom: 28. Apr., Seite 11-22 volume:50 year:2006 number:1 day:28 month:04 pages:11-22 |
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Enthalten in Current genetics 50(2006), 1 vom: 28. Apr., Seite 11-22 volume:50 year:2006 number:1 day:28 month:04 pages:11-22 |
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Miyazaki, Taiga @@aut@@ Tsai, Huei-Fung @@aut@@ Bennett, John E. @@aut@@ |
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S. cerevisiae Kre29p has been identified by affinity purification as a subunit of the Smc5–Smc6 complex, which is required for DNA repair and chromosome segregation. However, mutant phenotypes of S. cerevisiae KRE29 have not been well characterized and none of its orthologs’ functions has been reported. Here we report phenotypic characteristics of a C. glabratakre29 deletant. The absence of C. glabrata Kre29p resulted in decreased viability, exhibiting cell cycle arrest between late S-phase and metaphase even under normal growth conditions, and also caused an increase of plasmid loss rate, implying that Kre29p is required for mitotic chromosome transmission fidelity. The deletant showed increased sensitivity to high temperature as well as to DNA damaging agents including UV, gamma ray, 4-nitroquinoline-1-oxide and methyl methanesulfonate, and the phenotypes were restored in the KRE29 reintegrant. Consistent with the Δkre29 phenotypes, a Kre29p-GFP fusion protein was located in the nucleus. Furthermore, Kre29p-GFP became concentrated and formed distinct foci after exposure to 4-nitroquinoline-1-oxide. These results suggest the involvement of C. glabrata Kre29p in DNA repair. 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author |
Miyazaki, Taiga |
spellingShingle |
Miyazaki, Taiga misc DNA damage misc Cell cycle misc Mitosis misc Nucleus misc Plasmid partitioning Kre29p is a novel nuclear protein involved in DNA repair and mitotic fidelity in Candida glabrata |
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Kre29p is a novel nuclear protein involved in DNA repair and mitotic fidelity in Candida glabrata DNA damage (dpeaa)DE-He213 Cell cycle (dpeaa)DE-He213 Mitosis (dpeaa)DE-He213 Nucleus (dpeaa)DE-He213 Plasmid partitioning (dpeaa)DE-He213 |
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misc DNA damage misc Cell cycle misc Mitosis misc Nucleus misc Plasmid partitioning |
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Kre29p is a novel nuclear protein involved in DNA repair and mitotic fidelity in Candida glabrata |
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Kre29p is a novel nuclear protein involved in DNA repair and mitotic fidelity in Candida glabrata |
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Miyazaki, Taiga |
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Miyazaki, Taiga Tsai, Huei-Fung Bennett, John E. |
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10.1007/s00294-006-0072-3 |
title_sort |
kre29p is a novel nuclear protein involved in dna repair and mitotic fidelity in candida glabrata |
title_auth |
Kre29p is a novel nuclear protein involved in DNA repair and mitotic fidelity in Candida glabrata |
abstract |
Abstract Candida glabrata KRE29 is an ortholog of Saccharomyces cerevisiae KRE29. S. cerevisiae Kre29p has been identified by affinity purification as a subunit of the Smc5–Smc6 complex, which is required for DNA repair and chromosome segregation. However, mutant phenotypes of S. cerevisiae KRE29 have not been well characterized and none of its orthologs’ functions has been reported. Here we report phenotypic characteristics of a C. glabratakre29 deletant. The absence of C. glabrata Kre29p resulted in decreased viability, exhibiting cell cycle arrest between late S-phase and metaphase even under normal growth conditions, and also caused an increase of plasmid loss rate, implying that Kre29p is required for mitotic chromosome transmission fidelity. The deletant showed increased sensitivity to high temperature as well as to DNA damaging agents including UV, gamma ray, 4-nitroquinoline-1-oxide and methyl methanesulfonate, and the phenotypes were restored in the KRE29 reintegrant. Consistent with the Δkre29 phenotypes, a Kre29p-GFP fusion protein was located in the nucleus. Furthermore, Kre29p-GFP became concentrated and formed distinct foci after exposure to 4-nitroquinoline-1-oxide. These results suggest the involvement of C. glabrata Kre29p in DNA repair. To our knowledge, this is the first report addressing a cellular protein involved in DNA repair in C. glabrata. © Springer-Verlag 2006 |
abstractGer |
Abstract Candida glabrata KRE29 is an ortholog of Saccharomyces cerevisiae KRE29. S. cerevisiae Kre29p has been identified by affinity purification as a subunit of the Smc5–Smc6 complex, which is required for DNA repair and chromosome segregation. However, mutant phenotypes of S. cerevisiae KRE29 have not been well characterized and none of its orthologs’ functions has been reported. Here we report phenotypic characteristics of a C. glabratakre29 deletant. The absence of C. glabrata Kre29p resulted in decreased viability, exhibiting cell cycle arrest between late S-phase and metaphase even under normal growth conditions, and also caused an increase of plasmid loss rate, implying that Kre29p is required for mitotic chromosome transmission fidelity. The deletant showed increased sensitivity to high temperature as well as to DNA damaging agents including UV, gamma ray, 4-nitroquinoline-1-oxide and methyl methanesulfonate, and the phenotypes were restored in the KRE29 reintegrant. Consistent with the Δkre29 phenotypes, a Kre29p-GFP fusion protein was located in the nucleus. Furthermore, Kre29p-GFP became concentrated and formed distinct foci after exposure to 4-nitroquinoline-1-oxide. These results suggest the involvement of C. glabrata Kre29p in DNA repair. To our knowledge, this is the first report addressing a cellular protein involved in DNA repair in C. glabrata. © Springer-Verlag 2006 |
abstract_unstemmed |
Abstract Candida glabrata KRE29 is an ortholog of Saccharomyces cerevisiae KRE29. S. cerevisiae Kre29p has been identified by affinity purification as a subunit of the Smc5–Smc6 complex, which is required for DNA repair and chromosome segregation. However, mutant phenotypes of S. cerevisiae KRE29 have not been well characterized and none of its orthologs’ functions has been reported. Here we report phenotypic characteristics of a C. glabratakre29 deletant. The absence of C. glabrata Kre29p resulted in decreased viability, exhibiting cell cycle arrest between late S-phase and metaphase even under normal growth conditions, and also caused an increase of plasmid loss rate, implying that Kre29p is required for mitotic chromosome transmission fidelity. The deletant showed increased sensitivity to high temperature as well as to DNA damaging agents including UV, gamma ray, 4-nitroquinoline-1-oxide and methyl methanesulfonate, and the phenotypes were restored in the KRE29 reintegrant. Consistent with the Δkre29 phenotypes, a Kre29p-GFP fusion protein was located in the nucleus. Furthermore, Kre29p-GFP became concentrated and formed distinct foci after exposure to 4-nitroquinoline-1-oxide. These results suggest the involvement of C. glabrata Kre29p in DNA repair. To our knowledge, this is the first report addressing a cellular protein involved in DNA repair in C. glabrata. © Springer-Verlag 2006 |
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title_short |
Kre29p is a novel nuclear protein involved in DNA repair and mitotic fidelity in Candida glabrata |
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https://dx.doi.org/10.1007/s00294-006-0072-3 |
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Tsai, Huei-Fung Bennett, John E. |
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Tsai, Huei-Fung Bennett, John E. |
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10.1007/s00294-006-0072-3 |
up_date |
2024-07-03T21:49:23.457Z |
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score |
7.4002314 |