Functional relationships of FANCC to homologous recombination, translesion synthesis, and BLM
Abstract Some of the restarting events of stalled replication forks lead to sister chromatid exchange (SCE) as a result of homologous recombination (HR) repair with crossing over. The rate of SCE is elevated by the loss of BLM helicase or by a defect in translesion synthesis (TLS). We found that spo...
Ausführliche Beschreibung
Autor*in: |
Hirano, Seiki [verfasserIn] Yamamoto, Kazuhiko [verfasserIn] Ishiai, Masamichi [verfasserIn] Yamazoe, Mitsuyoshi [verfasserIn] Seki, Masayuki [verfasserIn] Matsushita, Nobuko [verfasserIn] Ohzeki, Mioko [verfasserIn] Yamashita, Yukiko M [verfasserIn] Arakawa, Hiroshi [verfasserIn] Buerstedde, Jean‐Marie [verfasserIn] Enomoto, Takemi [verfasserIn] Takeda, Shunichi [verfasserIn] Thompson, Larry H [verfasserIn] Takata, Minoru [verfasserIn] |
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E-Artikel |
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Sprache: |
Englisch |
Erschienen: |
2004 |
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Schlagwörter: |
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Anmerkung: |
© European Molecular Biology Organization 2005 |
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Übergeordnetes Werk: |
Enthalten in: The EMBO Journal - Nature Publishing Group UK, 2023, 24(2004), 2 vom: 23. Dez., Seite 418-427 |
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Übergeordnetes Werk: |
volume:24 ; year:2004 ; number:2 ; day:23 ; month:12 ; pages:418-427 |
Links: |
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DOI / URN: |
10.1038/sj.emboj.7600534 |
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Katalog-ID: |
SPR057950709 |
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100 | 1 | |a Hirano, Seiki |e verfasserin |4 aut | |
245 | 1 | 0 | |a Functional relationships of FANCC to homologous recombination, translesion synthesis, and BLM |
264 | 1 | |c 2004 | |
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520 | |a Abstract Some of the restarting events of stalled replication forks lead to sister chromatid exchange (SCE) as a result of homologous recombination (HR) repair with crossing over. The rate of SCE is elevated by the loss of BLM helicase or by a defect in translesion synthesis (TLS). We found that spontaneous SCE levels were elevated ∼2‐fold in chicken DT40 cells deficient in Fanconi anemia (FA) gene FANCC. To investigate the mechanism of the elevated SCE, we deleted FANCC in cells lacking Rad51 paralog XRCC3, TLS factor RAD18, or BLM. The increased SCE in fancc cells required Xrcc3, whereas the fancc/rad18 double mutant exhibited higher SCE than either single mutant. Unexpectedly, SCE in the fancc/blm mutant was similar to that in blm cells, indicating functional linkage between FANCC and BLM. Furthermore, MMC‐induced formation of GFP‐BLM nuclear foci was severely compromised in both human and chicken fancc or fancd2 cells. Our cell survival data suggest that the FA proteins serve to facilitate HR, but not global TLS, during crosslink repair. | ||
650 | 4 | |a Bloom syndrome |7 (dpeaa)DE-He213 | |
650 | 4 | |a Fanconi anemia |7 (dpeaa)DE-He213 | |
650 | 4 | |a homologous recombination |7 (dpeaa)DE-He213 | |
650 | 4 | |a sister chromatid exchange |7 (dpeaa)DE-He213 | |
650 | 4 | |a translesion synthesis |7 (dpeaa)DE-He213 | |
700 | 1 | |a Yamamoto, Kazuhiko |e verfasserin |4 aut | |
700 | 1 | |a Ishiai, Masamichi |e verfasserin |4 aut | |
700 | 1 | |a Yamazoe, Mitsuyoshi |e verfasserin |4 aut | |
700 | 1 | |a Seki, Masayuki |e verfasserin |4 aut | |
700 | 1 | |a Matsushita, Nobuko |e verfasserin |4 aut | |
700 | 1 | |a Ohzeki, Mioko |e verfasserin |4 aut | |
700 | 1 | |a Yamashita, Yukiko M |e verfasserin |4 aut | |
700 | 1 | |a Arakawa, Hiroshi |e verfasserin |4 aut | |
700 | 1 | |a Buerstedde, Jean‐Marie |e verfasserin |4 aut | |
700 | 1 | |a Enomoto, Takemi |e verfasserin |4 aut | |
700 | 1 | |a Takeda, Shunichi |e verfasserin |4 aut | |
700 | 1 | |a Thompson, Larry H |e verfasserin |4 aut | |
700 | 1 | |a Takata, Minoru |e verfasserin |4 aut | |
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773 | 1 | 8 | |g volume:24 |g year:2004 |g number:2 |g day:23 |g month:12 |g pages:418-427 |
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2004 |
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10.1038/sj.emboj.7600534 doi (DE-627)SPR057950709 (SPR)sj.emboj.7600534-e DE-627 ger DE-627 rakwb eng Hirano, Seiki verfasserin aut Functional relationships of FANCC to homologous recombination, translesion synthesis, and BLM 2004 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © European Molecular Biology Organization 2005 Abstract Some of the restarting events of stalled replication forks lead to sister chromatid exchange (SCE) as a result of homologous recombination (HR) repair with crossing over. The rate of SCE is elevated by the loss of BLM helicase or by a defect in translesion synthesis (TLS). We found that spontaneous SCE levels were elevated ∼2‐fold in chicken DT40 cells deficient in Fanconi anemia (FA) gene FANCC. To investigate the mechanism of the elevated SCE, we deleted FANCC in cells lacking Rad51 paralog XRCC3, TLS factor RAD18, or BLM. The increased SCE in fancc cells required Xrcc3, whereas the fancc/rad18 double mutant exhibited higher SCE than either single mutant. Unexpectedly, SCE in the fancc/blm mutant was similar to that in blm cells, indicating functional linkage between FANCC and BLM. Furthermore, MMC‐induced formation of GFP‐BLM nuclear foci was severely compromised in both human and chicken fancc or fancd2 cells. Our cell survival data suggest that the FA proteins serve to facilitate HR, but not global TLS, during crosslink repair. Bloom syndrome (dpeaa)DE-He213 Fanconi anemia (dpeaa)DE-He213 homologous recombination (dpeaa)DE-He213 sister chromatid exchange (dpeaa)DE-He213 translesion synthesis (dpeaa)DE-He213 Yamamoto, Kazuhiko verfasserin aut Ishiai, Masamichi verfasserin aut Yamazoe, Mitsuyoshi verfasserin aut Seki, Masayuki verfasserin aut Matsushita, Nobuko verfasserin aut Ohzeki, Mioko verfasserin aut Yamashita, Yukiko M verfasserin aut Arakawa, Hiroshi verfasserin aut Buerstedde, Jean‐Marie verfasserin aut Enomoto, Takemi verfasserin aut Takeda, Shunichi verfasserin aut Thompson, Larry H verfasserin aut Takata, Minoru verfasserin aut Enthalten in The EMBO Journal Nature Publishing Group UK, 2023 24(2004), 2 vom: 23. Dez., Seite 418-427 (DE-627)266022529 (DE-600)1467419-1 1460-2075 nnns volume:24 year:2004 number:2 day:23 month:12 pages:418-427 https://dx.doi.org/10.1038/sj.emboj.7600534 X:SPRINGER Resolving-System lizenzpflichtig Volltext SYSFLAG_0 GBV_SPRINGER 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_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_72 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_168 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_252 GBV_ILN_266 GBV_ILN_285 GBV_ILN_293 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_2018 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2113 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_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4029 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4116 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4155 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4311 GBV_ILN_4313 GBV_ILN_4314 GBV_ILN_4318 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4598 GBV_ILN_4700 AR 24 2004 2 23 12 418-427 |
spelling |
10.1038/sj.emboj.7600534 doi (DE-627)SPR057950709 (SPR)sj.emboj.7600534-e DE-627 ger DE-627 rakwb eng Hirano, Seiki verfasserin aut Functional relationships of FANCC to homologous recombination, translesion synthesis, and BLM 2004 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © European Molecular Biology Organization 2005 Abstract Some of the restarting events of stalled replication forks lead to sister chromatid exchange (SCE) as a result of homologous recombination (HR) repair with crossing over. The rate of SCE is elevated by the loss of BLM helicase or by a defect in translesion synthesis (TLS). We found that spontaneous SCE levels were elevated ∼2‐fold in chicken DT40 cells deficient in Fanconi anemia (FA) gene FANCC. To investigate the mechanism of the elevated SCE, we deleted FANCC in cells lacking Rad51 paralog XRCC3, TLS factor RAD18, or BLM. The increased SCE in fancc cells required Xrcc3, whereas the fancc/rad18 double mutant exhibited higher SCE than either single mutant. Unexpectedly, SCE in the fancc/blm mutant was similar to that in blm cells, indicating functional linkage between FANCC and BLM. Furthermore, MMC‐induced formation of GFP‐BLM nuclear foci was severely compromised in both human and chicken fancc or fancd2 cells. Our cell survival data suggest that the FA proteins serve to facilitate HR, but not global TLS, during crosslink repair. Bloom syndrome (dpeaa)DE-He213 Fanconi anemia (dpeaa)DE-He213 homologous recombination (dpeaa)DE-He213 sister chromatid exchange (dpeaa)DE-He213 translesion synthesis (dpeaa)DE-He213 Yamamoto, Kazuhiko verfasserin aut Ishiai, Masamichi verfasserin aut Yamazoe, Mitsuyoshi verfasserin aut Seki, Masayuki verfasserin aut Matsushita, Nobuko verfasserin aut Ohzeki, Mioko verfasserin aut Yamashita, Yukiko M verfasserin aut Arakawa, Hiroshi verfasserin aut Buerstedde, Jean‐Marie verfasserin aut Enomoto, Takemi verfasserin aut Takeda, Shunichi verfasserin aut Thompson, Larry H verfasserin aut Takata, Minoru verfasserin aut Enthalten in The EMBO Journal Nature Publishing Group UK, 2023 24(2004), 2 vom: 23. Dez., Seite 418-427 (DE-627)266022529 (DE-600)1467419-1 1460-2075 nnns volume:24 year:2004 number:2 day:23 month:12 pages:418-427 https://dx.doi.org/10.1038/sj.emboj.7600534 X:SPRINGER Resolving-System lizenzpflichtig Volltext SYSFLAG_0 GBV_SPRINGER 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_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_72 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_168 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_252 GBV_ILN_266 GBV_ILN_285 GBV_ILN_293 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_2018 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2113 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_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4029 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4116 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4155 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4311 GBV_ILN_4313 GBV_ILN_4314 GBV_ILN_4318 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4598 GBV_ILN_4700 AR 24 2004 2 23 12 418-427 |
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10.1038/sj.emboj.7600534 doi (DE-627)SPR057950709 (SPR)sj.emboj.7600534-e DE-627 ger DE-627 rakwb eng Hirano, Seiki verfasserin aut Functional relationships of FANCC to homologous recombination, translesion synthesis, and BLM 2004 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © European Molecular Biology Organization 2005 Abstract Some of the restarting events of stalled replication forks lead to sister chromatid exchange (SCE) as a result of homologous recombination (HR) repair with crossing over. The rate of SCE is elevated by the loss of BLM helicase or by a defect in translesion synthesis (TLS). We found that spontaneous SCE levels were elevated ∼2‐fold in chicken DT40 cells deficient in Fanconi anemia (FA) gene FANCC. To investigate the mechanism of the elevated SCE, we deleted FANCC in cells lacking Rad51 paralog XRCC3, TLS factor RAD18, or BLM. The increased SCE in fancc cells required Xrcc3, whereas the fancc/rad18 double mutant exhibited higher SCE than either single mutant. Unexpectedly, SCE in the fancc/blm mutant was similar to that in blm cells, indicating functional linkage between FANCC and BLM. Furthermore, MMC‐induced formation of GFP‐BLM nuclear foci was severely compromised in both human and chicken fancc or fancd2 cells. Our cell survival data suggest that the FA proteins serve to facilitate HR, but not global TLS, during crosslink repair. Bloom syndrome (dpeaa)DE-He213 Fanconi anemia (dpeaa)DE-He213 homologous recombination (dpeaa)DE-He213 sister chromatid exchange (dpeaa)DE-He213 translesion synthesis (dpeaa)DE-He213 Yamamoto, Kazuhiko verfasserin aut Ishiai, Masamichi verfasserin aut Yamazoe, Mitsuyoshi verfasserin aut Seki, Masayuki verfasserin aut Matsushita, Nobuko verfasserin aut Ohzeki, Mioko verfasserin aut Yamashita, Yukiko M verfasserin aut Arakawa, Hiroshi verfasserin aut Buerstedde, Jean‐Marie verfasserin aut Enomoto, Takemi verfasserin aut Takeda, Shunichi verfasserin aut Thompson, Larry H verfasserin aut Takata, Minoru verfasserin aut Enthalten in The EMBO Journal Nature Publishing Group UK, 2023 24(2004), 2 vom: 23. Dez., Seite 418-427 (DE-627)266022529 (DE-600)1467419-1 1460-2075 nnns volume:24 year:2004 number:2 day:23 month:12 pages:418-427 https://dx.doi.org/10.1038/sj.emboj.7600534 X:SPRINGER Resolving-System lizenzpflichtig Volltext SYSFLAG_0 GBV_SPRINGER 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_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_72 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_168 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_252 GBV_ILN_266 GBV_ILN_285 GBV_ILN_293 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_2018 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2113 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_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4029 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4116 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4155 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4311 GBV_ILN_4313 GBV_ILN_4314 GBV_ILN_4318 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4598 GBV_ILN_4700 AR 24 2004 2 23 12 418-427 |
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10.1038/sj.emboj.7600534 doi (DE-627)SPR057950709 (SPR)sj.emboj.7600534-e DE-627 ger DE-627 rakwb eng Hirano, Seiki verfasserin aut Functional relationships of FANCC to homologous recombination, translesion synthesis, and BLM 2004 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © European Molecular Biology Organization 2005 Abstract Some of the restarting events of stalled replication forks lead to sister chromatid exchange (SCE) as a result of homologous recombination (HR) repair with crossing over. The rate of SCE is elevated by the loss of BLM helicase or by a defect in translesion synthesis (TLS). We found that spontaneous SCE levels were elevated ∼2‐fold in chicken DT40 cells deficient in Fanconi anemia (FA) gene FANCC. To investigate the mechanism of the elevated SCE, we deleted FANCC in cells lacking Rad51 paralog XRCC3, TLS factor RAD18, or BLM. The increased SCE in fancc cells required Xrcc3, whereas the fancc/rad18 double mutant exhibited higher SCE than either single mutant. Unexpectedly, SCE in the fancc/blm mutant was similar to that in blm cells, indicating functional linkage between FANCC and BLM. Furthermore, MMC‐induced formation of GFP‐BLM nuclear foci was severely compromised in both human and chicken fancc or fancd2 cells. Our cell survival data suggest that the FA proteins serve to facilitate HR, but not global TLS, during crosslink repair. Bloom syndrome (dpeaa)DE-He213 Fanconi anemia (dpeaa)DE-He213 homologous recombination (dpeaa)DE-He213 sister chromatid exchange (dpeaa)DE-He213 translesion synthesis (dpeaa)DE-He213 Yamamoto, Kazuhiko verfasserin aut Ishiai, Masamichi verfasserin aut Yamazoe, Mitsuyoshi verfasserin aut Seki, Masayuki verfasserin aut Matsushita, Nobuko verfasserin aut Ohzeki, Mioko verfasserin aut Yamashita, Yukiko M verfasserin aut Arakawa, Hiroshi verfasserin aut Buerstedde, Jean‐Marie verfasserin aut Enomoto, Takemi verfasserin aut Takeda, Shunichi verfasserin aut Thompson, Larry H verfasserin aut Takata, Minoru verfasserin aut Enthalten in The EMBO Journal Nature Publishing Group UK, 2023 24(2004), 2 vom: 23. Dez., Seite 418-427 (DE-627)266022529 (DE-600)1467419-1 1460-2075 nnns volume:24 year:2004 number:2 day:23 month:12 pages:418-427 https://dx.doi.org/10.1038/sj.emboj.7600534 X:SPRINGER Resolving-System lizenzpflichtig Volltext SYSFLAG_0 GBV_SPRINGER 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_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_72 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_168 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_252 GBV_ILN_266 GBV_ILN_285 GBV_ILN_293 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_2018 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2113 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_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4029 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4116 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4155 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4311 GBV_ILN_4313 GBV_ILN_4314 GBV_ILN_4318 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4598 GBV_ILN_4700 AR 24 2004 2 23 12 418-427 |
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10.1038/sj.emboj.7600534 doi (DE-627)SPR057950709 (SPR)sj.emboj.7600534-e DE-627 ger DE-627 rakwb eng Hirano, Seiki verfasserin aut Functional relationships of FANCC to homologous recombination, translesion synthesis, and BLM 2004 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © European Molecular Biology Organization 2005 Abstract Some of the restarting events of stalled replication forks lead to sister chromatid exchange (SCE) as a result of homologous recombination (HR) repair with crossing over. The rate of SCE is elevated by the loss of BLM helicase or by a defect in translesion synthesis (TLS). We found that spontaneous SCE levels were elevated ∼2‐fold in chicken DT40 cells deficient in Fanconi anemia (FA) gene FANCC. To investigate the mechanism of the elevated SCE, we deleted FANCC in cells lacking Rad51 paralog XRCC3, TLS factor RAD18, or BLM. The increased SCE in fancc cells required Xrcc3, whereas the fancc/rad18 double mutant exhibited higher SCE than either single mutant. Unexpectedly, SCE in the fancc/blm mutant was similar to that in blm cells, indicating functional linkage between FANCC and BLM. Furthermore, MMC‐induced formation of GFP‐BLM nuclear foci was severely compromised in both human and chicken fancc or fancd2 cells. Our cell survival data suggest that the FA proteins serve to facilitate HR, but not global TLS, during crosslink repair. Bloom syndrome (dpeaa)DE-He213 Fanconi anemia (dpeaa)DE-He213 homologous recombination (dpeaa)DE-He213 sister chromatid exchange (dpeaa)DE-He213 translesion synthesis (dpeaa)DE-He213 Yamamoto, Kazuhiko verfasserin aut Ishiai, Masamichi verfasserin aut Yamazoe, Mitsuyoshi verfasserin aut Seki, Masayuki verfasserin aut Matsushita, Nobuko verfasserin aut Ohzeki, Mioko verfasserin aut Yamashita, Yukiko M verfasserin aut Arakawa, Hiroshi verfasserin aut Buerstedde, Jean‐Marie verfasserin aut Enomoto, Takemi verfasserin aut Takeda, Shunichi verfasserin aut Thompson, Larry H verfasserin aut Takata, Minoru verfasserin aut Enthalten in The EMBO Journal Nature Publishing Group UK, 2023 24(2004), 2 vom: 23. Dez., Seite 418-427 (DE-627)266022529 (DE-600)1467419-1 1460-2075 nnns volume:24 year:2004 number:2 day:23 month:12 pages:418-427 https://dx.doi.org/10.1038/sj.emboj.7600534 X:SPRINGER Resolving-System lizenzpflichtig Volltext SYSFLAG_0 GBV_SPRINGER 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_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_72 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_168 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_252 GBV_ILN_266 GBV_ILN_285 GBV_ILN_293 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_2018 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2113 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_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4029 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4116 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4155 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4311 GBV_ILN_4313 GBV_ILN_4314 GBV_ILN_4318 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4598 GBV_ILN_4700 AR 24 2004 2 23 12 418-427 |
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Enthalten in The EMBO Journal 24(2004), 2 vom: 23. Dez., Seite 418-427 volume:24 year:2004 number:2 day:23 month:12 pages:418-427 |
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Enthalten in The EMBO Journal 24(2004), 2 vom: 23. Dez., Seite 418-427 volume:24 year:2004 number:2 day:23 month:12 pages:418-427 |
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Bloom syndrome Fanconi anemia homologous recombination sister chromatid exchange translesion synthesis |
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Hirano, Seiki @@aut@@ Yamamoto, Kazuhiko @@aut@@ Ishiai, Masamichi @@aut@@ Yamazoe, Mitsuyoshi @@aut@@ Seki, Masayuki @@aut@@ Matsushita, Nobuko @@aut@@ Ohzeki, Mioko @@aut@@ Yamashita, Yukiko M @@aut@@ Arakawa, Hiroshi @@aut@@ Buerstedde, Jean‐Marie @@aut@@ Enomoto, Takemi @@aut@@ Takeda, Shunichi @@aut@@ Thompson, Larry H @@aut@@ Takata, Minoru @@aut@@ |
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The rate of SCE is elevated by the loss of BLM helicase or by a defect in translesion synthesis (TLS). We found that spontaneous SCE levels were elevated ∼2‐fold in chicken DT40 cells deficient in Fanconi anemia (FA) gene FANCC. To investigate the mechanism of the elevated SCE, we deleted FANCC in cells lacking Rad51 paralog XRCC3, TLS factor RAD18, or BLM. The increased SCE in fancc cells required Xrcc3, whereas the fancc/rad18 double mutant exhibited higher SCE than either single mutant. Unexpectedly, SCE in the fancc/blm mutant was similar to that in blm cells, indicating functional linkage between FANCC and BLM. Furthermore, MMC‐induced formation of GFP‐BLM nuclear foci was severely compromised in both human and chicken fancc or fancd2 cells. 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Hirano, Seiki |
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Hirano, Seiki misc Bloom syndrome misc Fanconi anemia misc homologous recombination misc sister chromatid exchange misc translesion synthesis Functional relationships of FANCC to homologous recombination, translesion synthesis, and BLM |
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Functional relationships of FANCC to homologous recombination, translesion synthesis, and BLM Bloom syndrome (dpeaa)DE-He213 Fanconi anemia (dpeaa)DE-He213 homologous recombination (dpeaa)DE-He213 sister chromatid exchange (dpeaa)DE-He213 translesion synthesis (dpeaa)DE-He213 |
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Hirano, Seiki Yamamoto, Kazuhiko Ishiai, Masamichi Yamazoe, Mitsuyoshi Seki, Masayuki Matsushita, Nobuko Ohzeki, Mioko Yamashita, Yukiko M Arakawa, Hiroshi Buerstedde, Jean‐Marie Enomoto, Takemi Takeda, Shunichi Thompson, Larry H Takata, Minoru |
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Elektronische Aufsätze |
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functional relationships of fancc to homologous recombination, translesion synthesis, and blm |
title_auth |
Functional relationships of FANCC to homologous recombination, translesion synthesis, and BLM |
abstract |
Abstract Some of the restarting events of stalled replication forks lead to sister chromatid exchange (SCE) as a result of homologous recombination (HR) repair with crossing over. The rate of SCE is elevated by the loss of BLM helicase or by a defect in translesion synthesis (TLS). We found that spontaneous SCE levels were elevated ∼2‐fold in chicken DT40 cells deficient in Fanconi anemia (FA) gene FANCC. To investigate the mechanism of the elevated SCE, we deleted FANCC in cells lacking Rad51 paralog XRCC3, TLS factor RAD18, or BLM. The increased SCE in fancc cells required Xrcc3, whereas the fancc/rad18 double mutant exhibited higher SCE than either single mutant. Unexpectedly, SCE in the fancc/blm mutant was similar to that in blm cells, indicating functional linkage between FANCC and BLM. Furthermore, MMC‐induced formation of GFP‐BLM nuclear foci was severely compromised in both human and chicken fancc or fancd2 cells. Our cell survival data suggest that the FA proteins serve to facilitate HR, but not global TLS, during crosslink repair. © European Molecular Biology Organization 2005 |
abstractGer |
Abstract Some of the restarting events of stalled replication forks lead to sister chromatid exchange (SCE) as a result of homologous recombination (HR) repair with crossing over. The rate of SCE is elevated by the loss of BLM helicase or by a defect in translesion synthesis (TLS). We found that spontaneous SCE levels were elevated ∼2‐fold in chicken DT40 cells deficient in Fanconi anemia (FA) gene FANCC. To investigate the mechanism of the elevated SCE, we deleted FANCC in cells lacking Rad51 paralog XRCC3, TLS factor RAD18, or BLM. The increased SCE in fancc cells required Xrcc3, whereas the fancc/rad18 double mutant exhibited higher SCE than either single mutant. Unexpectedly, SCE in the fancc/blm mutant was similar to that in blm cells, indicating functional linkage between FANCC and BLM. Furthermore, MMC‐induced formation of GFP‐BLM nuclear foci was severely compromised in both human and chicken fancc or fancd2 cells. Our cell survival data suggest that the FA proteins serve to facilitate HR, but not global TLS, during crosslink repair. © European Molecular Biology Organization 2005 |
abstract_unstemmed |
Abstract Some of the restarting events of stalled replication forks lead to sister chromatid exchange (SCE) as a result of homologous recombination (HR) repair with crossing over. The rate of SCE is elevated by the loss of BLM helicase or by a defect in translesion synthesis (TLS). We found that spontaneous SCE levels were elevated ∼2‐fold in chicken DT40 cells deficient in Fanconi anemia (FA) gene FANCC. To investigate the mechanism of the elevated SCE, we deleted FANCC in cells lacking Rad51 paralog XRCC3, TLS factor RAD18, or BLM. The increased SCE in fancc cells required Xrcc3, whereas the fancc/rad18 double mutant exhibited higher SCE than either single mutant. Unexpectedly, SCE in the fancc/blm mutant was similar to that in blm cells, indicating functional linkage between FANCC and BLM. Furthermore, MMC‐induced formation of GFP‐BLM nuclear foci was severely compromised in both human and chicken fancc or fancd2 cells. Our cell survival data suggest that the FA proteins serve to facilitate HR, but not global TLS, during crosslink repair. © European Molecular Biology Organization 2005 |
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title_short |
Functional relationships of FANCC to homologous recombination, translesion synthesis, and BLM |
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https://dx.doi.org/10.1038/sj.emboj.7600534 |
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Yamamoto, Kazuhiko Ishiai, Masamichi Yamazoe, Mitsuyoshi Seki, Masayuki Matsushita, Nobuko Ohzeki, Mioko Yamashita, Yukiko M Arakawa, Hiroshi Buerstedde, Jean‐Marie Enomoto, Takemi Takeda, Shunichi Thompson, Larry H Takata, Minoru |
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Yamamoto, Kazuhiko Ishiai, Masamichi Yamazoe, Mitsuyoshi Seki, Masayuki Matsushita, Nobuko Ohzeki, Mioko Yamashita, Yukiko M Arakawa, Hiroshi Buerstedde, Jean‐Marie Enomoto, Takemi Takeda, Shunichi Thompson, Larry H Takata, Minoru |
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score |
7.4002237 |