Arabidopsis RETINOBLASTOMA RELATED directly regulates DNA damage responses through functions beyond cell cycle control
Abstract The rapidly proliferating cells in plant meristems must be protected from genome damage. Here, we show that the regulatory role of the Arabidopsis RETINOBLASTOMA RELATED (RBR) in cell proliferation can be separated from a novel function in safeguarding genome integrity. Upon DNA damage, RBR...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Horvath, Beatrix M [verfasserIn] Kourova, Hana [verfasserIn] Nagy, Szilvia [verfasserIn] Nemeth, Edit [verfasserIn] Magyar, Zoltan [verfasserIn] Papdi, Csaba [verfasserIn] Ahmad, Zaki [verfasserIn] Sanchez‐Perez, Gabino F [verfasserIn] Perilli, Serena [verfasserIn] Blilou, Ikram [verfasserIn] Pettkó‐Szandtner, Aladár [verfasserIn] Darula, Zsuzsanna [verfasserIn] Meszaros, Tamas [verfasserIn] Binarova, Pavla [verfasserIn] Bogre, Laszlo [verfasserIn] Scheres, Ben [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2017 |
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| Schlagwörter: |
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| Anmerkung: |
© The Authors. Published under the terms of the CC BY 4.0 license 2017 |
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| Übergeordnetes Werk: |
Enthalten in: The EMBO Journal - Nature Publishing Group UK, 2023, 36(2017), 9 vom: 20. März, Seite 1261-1278 |
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| Übergeordnetes Werk: |
volume:36 ; year:2017 ; number:9 ; day:20 ; month:03 ; pages:1261-1278 |
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| DOI / URN: |
10.15252/embj.201694561 |
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| Katalog-ID: |
SPR057871922 |
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| 100 | 1 | |a Horvath, Beatrix M |e verfasserin |0 (orcid)0000-0002-6083-992X |4 aut | |
| 245 | 1 | 0 | |a Arabidopsis RETINOBLASTOMA RELATED directly regulates DNA damage responses through functions beyond cell cycle control |
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| 500 | |a © The Authors. Published under the terms of the CC BY 4.0 license 2017 | ||
| 520 | |a Abstract The rapidly proliferating cells in plant meristems must be protected from genome damage. Here, we show that the regulatory role of the Arabidopsis RETINOBLASTOMA RELATED (RBR) in cell proliferation can be separated from a novel function in safeguarding genome integrity. Upon DNA damage, RBR and its binding partner E2FA are recruited to heterochromatic γH2AX‐labelled DNA damage foci in an ATM‐ and ATR‐dependent manner. These γH2AX‐labelled DNA lesions are more dispersedly occupied by the conserved repair protein, AtBRCA1, which can also co‐localise with RBR foci. RBR and AtBRCA1 physically interact in vitro and in planta. Genetic interaction between the RBR‐silenced amiRBR and Atbrca1 mutants suggests that RBR and AtBRCA1 may function together in maintaining genome integrity. Together with E2FA, RBR is directly involved in the transcriptional DNA damage response as well as in the cell death pathway that is independent of SOG1, the plant functional analogue of p53. Thus, plant homologs and analogues of major mammalian tumour suppressor proteins form a regulatory network that coordinates cell proliferation with cell and genome integrity. | ||
| 520 | |a Synopsis Arabidopsis RETINOBLASTOMA RELATED (RBR), the plant homolog of the mammalian retinoblastoma tumor suppressor protein, transcriptionally regulates damage response and cell death pathways, but also directly cooperates with the repair factor BRCA1 to maintain genome integrity after damage. Beyond its role in cell cycle control, RBR has a function in maintaining genome integrity and cell viability.RBR together with E2FA frequently accumulates on γH2AX‐labelled damage foci during DNA damage responses.RBR and AtBRCA1 physically interact and co‐localise on a subset of γH2AX‐labelled nuclear foci.Genetic interactions of RBR and AtBRCA1 support their synergistic action in DNA repair.RBR and E2FA regulate AtBRCA1 transcription and cell death responses in a SOG1‐independent pathway. | ||
| 520 | |a Graphical Abstract The tumor suppressor plant homolog transcriptionally regulates damage response and cell death pathways, but also directly cooperates with the repair factor BRCA1 to maintain genome integrity after damage. | ||
| 650 | 4 | |a BRCA1 |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a DNA damage response |7 (dpeaa)DE-He213 | |
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| 650 | 4 | |a RETINOBLASTOMA RELATED |7 (dpeaa)DE-He213 | |
| 700 | 1 | |a Kourova, Hana |e verfasserin |4 aut | |
| 700 | 1 | |a Nagy, Szilvia |e verfasserin |4 aut | |
| 700 | 1 | |a Nemeth, Edit |e verfasserin |0 (orcid)0000-0002-9233-0773 |4 aut | |
| 700 | 1 | |a Magyar, Zoltan |e verfasserin |4 aut | |
| 700 | 1 | |a Papdi, Csaba |e verfasserin |0 (orcid)0000-0003-0640-6098 |4 aut | |
| 700 | 1 | |a Ahmad, Zaki |e verfasserin |0 (orcid)0000-0002-0258-704X |4 aut | |
| 700 | 1 | |a Sanchez‐Perez, Gabino F |e verfasserin |4 aut | |
| 700 | 1 | |a Perilli, Serena |e verfasserin |4 aut | |
| 700 | 1 | |a Blilou, Ikram |e verfasserin |4 aut | |
| 700 | 1 | |a Pettkó‐Szandtner, Aladár |e verfasserin |4 aut | |
| 700 | 1 | |a Darula, Zsuzsanna |e verfasserin |4 aut | |
| 700 | 1 | |a Meszaros, Tamas |e verfasserin |4 aut | |
| 700 | 1 | |a Binarova, Pavla |e verfasserin |4 aut | |
| 700 | 1 | |a Bogre, Laszlo |e verfasserin |4 aut | |
| 700 | 1 | |a Scheres, Ben |e verfasserin |0 (orcid)0000-0001-5400-9578 |4 aut | |
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10.15252/embj.201694561 doi (DE-627)SPR057871922 (SPR)embj.201694561-e DE-627 ger DE-627 rakwb eng Horvath, Beatrix M verfasserin (orcid)0000-0002-6083-992X aut Arabidopsis RETINOBLASTOMA RELATED directly regulates DNA damage responses through functions beyond cell cycle control 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Authors. Published under the terms of the CC BY 4.0 license 2017 Abstract The rapidly proliferating cells in plant meristems must be protected from genome damage. Here, we show that the regulatory role of the Arabidopsis RETINOBLASTOMA RELATED (RBR) in cell proliferation can be separated from a novel function in safeguarding genome integrity. Upon DNA damage, RBR and its binding partner E2FA are recruited to heterochromatic γH2AX‐labelled DNA damage foci in an ATM‐ and ATR‐dependent manner. These γH2AX‐labelled DNA lesions are more dispersedly occupied by the conserved repair protein, AtBRCA1, which can also co‐localise with RBR foci. RBR and AtBRCA1 physically interact in vitro and in planta. Genetic interaction between the RBR‐silenced amiRBR and Atbrca1 mutants suggests that RBR and AtBRCA1 may function together in maintaining genome integrity. Together with E2FA, RBR is directly involved in the transcriptional DNA damage response as well as in the cell death pathway that is independent of SOG1, the plant functional analogue of p53. Thus, plant homologs and analogues of major mammalian tumour suppressor proteins form a regulatory network that coordinates cell proliferation with cell and genome integrity. Synopsis Arabidopsis RETINOBLASTOMA RELATED (RBR), the plant homolog of the mammalian retinoblastoma tumor suppressor protein, transcriptionally regulates damage response and cell death pathways, but also directly cooperates with the repair factor BRCA1 to maintain genome integrity after damage. Beyond its role in cell cycle control, RBR has a function in maintaining genome integrity and cell viability.RBR together with E2FA frequently accumulates on γH2AX‐labelled damage foci during DNA damage responses.RBR and AtBRCA1 physically interact and co‐localise on a subset of γH2AX‐labelled nuclear foci.Genetic interactions of RBR and AtBRCA1 support their synergistic action in DNA repair.RBR and E2FA regulate AtBRCA1 transcription and cell death responses in a SOG1‐independent pathway. Graphical Abstract The tumor suppressor plant homolog transcriptionally regulates damage response and cell death pathways, but also directly cooperates with the repair factor BRCA1 to maintain genome integrity after damage. BRCA1 (dpeaa)DE-He213 DNA damage response (dpeaa)DE-He213 E2FA (dpeaa)DE-He213 RETINOBLASTOMA RELATED (dpeaa)DE-He213 Kourova, Hana verfasserin aut Nagy, Szilvia verfasserin aut Nemeth, Edit verfasserin (orcid)0000-0002-9233-0773 aut Magyar, Zoltan verfasserin aut Papdi, Csaba verfasserin (orcid)0000-0003-0640-6098 aut Ahmad, Zaki verfasserin (orcid)0000-0002-0258-704X aut Sanchez‐Perez, Gabino F verfasserin aut Perilli, Serena verfasserin aut Blilou, Ikram verfasserin aut Pettkó‐Szandtner, Aladár verfasserin aut Darula, Zsuzsanna verfasserin aut Meszaros, Tamas verfasserin aut Binarova, Pavla verfasserin aut Bogre, Laszlo verfasserin aut Scheres, Ben verfasserin (orcid)0000-0001-5400-9578 aut Enthalten in The EMBO Journal Nature Publishing Group UK, 2023 36(2017), 9 vom: 20. März, Seite 1261-1278 (DE-627)266022529 (DE-600)1467419-1 1460-2075 nnns volume:36 year:2017 number:9 day:20 month:03 pages:1261-1278 https://dx.doi.org/10.15252/embj.201694561 X:SPRINGER Resolving-System kostenfrei 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_211 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_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_4313 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_4700 AR 36 2017 9 20 03 1261-1278 |
| spelling |
10.15252/embj.201694561 doi (DE-627)SPR057871922 (SPR)embj.201694561-e DE-627 ger DE-627 rakwb eng Horvath, Beatrix M verfasserin (orcid)0000-0002-6083-992X aut Arabidopsis RETINOBLASTOMA RELATED directly regulates DNA damage responses through functions beyond cell cycle control 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Authors. Published under the terms of the CC BY 4.0 license 2017 Abstract The rapidly proliferating cells in plant meristems must be protected from genome damage. Here, we show that the regulatory role of the Arabidopsis RETINOBLASTOMA RELATED (RBR) in cell proliferation can be separated from a novel function in safeguarding genome integrity. Upon DNA damage, RBR and its binding partner E2FA are recruited to heterochromatic γH2AX‐labelled DNA damage foci in an ATM‐ and ATR‐dependent manner. These γH2AX‐labelled DNA lesions are more dispersedly occupied by the conserved repair protein, AtBRCA1, which can also co‐localise with RBR foci. RBR and AtBRCA1 physically interact in vitro and in planta. Genetic interaction between the RBR‐silenced amiRBR and Atbrca1 mutants suggests that RBR and AtBRCA1 may function together in maintaining genome integrity. Together with E2FA, RBR is directly involved in the transcriptional DNA damage response as well as in the cell death pathway that is independent of SOG1, the plant functional analogue of p53. Thus, plant homologs and analogues of major mammalian tumour suppressor proteins form a regulatory network that coordinates cell proliferation with cell and genome integrity. Synopsis Arabidopsis RETINOBLASTOMA RELATED (RBR), the plant homolog of the mammalian retinoblastoma tumor suppressor protein, transcriptionally regulates damage response and cell death pathways, but also directly cooperates with the repair factor BRCA1 to maintain genome integrity after damage. Beyond its role in cell cycle control, RBR has a function in maintaining genome integrity and cell viability.RBR together with E2FA frequently accumulates on γH2AX‐labelled damage foci during DNA damage responses.RBR and AtBRCA1 physically interact and co‐localise on a subset of γH2AX‐labelled nuclear foci.Genetic interactions of RBR and AtBRCA1 support their synergistic action in DNA repair.RBR and E2FA regulate AtBRCA1 transcription and cell death responses in a SOG1‐independent pathway. Graphical Abstract The tumor suppressor plant homolog transcriptionally regulates damage response and cell death pathways, but also directly cooperates with the repair factor BRCA1 to maintain genome integrity after damage. BRCA1 (dpeaa)DE-He213 DNA damage response (dpeaa)DE-He213 E2FA (dpeaa)DE-He213 RETINOBLASTOMA RELATED (dpeaa)DE-He213 Kourova, Hana verfasserin aut Nagy, Szilvia verfasserin aut Nemeth, Edit verfasserin (orcid)0000-0002-9233-0773 aut Magyar, Zoltan verfasserin aut Papdi, Csaba verfasserin (orcid)0000-0003-0640-6098 aut Ahmad, Zaki verfasserin (orcid)0000-0002-0258-704X aut Sanchez‐Perez, Gabino F verfasserin aut Perilli, Serena verfasserin aut Blilou, Ikram verfasserin aut Pettkó‐Szandtner, Aladár verfasserin aut Darula, Zsuzsanna verfasserin aut Meszaros, Tamas verfasserin aut Binarova, Pavla verfasserin aut Bogre, Laszlo verfasserin aut Scheres, Ben verfasserin (orcid)0000-0001-5400-9578 aut Enthalten in The EMBO Journal Nature Publishing Group UK, 2023 36(2017), 9 vom: 20. März, Seite 1261-1278 (DE-627)266022529 (DE-600)1467419-1 1460-2075 nnns volume:36 year:2017 number:9 day:20 month:03 pages:1261-1278 https://dx.doi.org/10.15252/embj.201694561 X:SPRINGER Resolving-System kostenfrei 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_211 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_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_4313 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_4700 AR 36 2017 9 20 03 1261-1278 |
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10.15252/embj.201694561 doi (DE-627)SPR057871922 (SPR)embj.201694561-e DE-627 ger DE-627 rakwb eng Horvath, Beatrix M verfasserin (orcid)0000-0002-6083-992X aut Arabidopsis RETINOBLASTOMA RELATED directly regulates DNA damage responses through functions beyond cell cycle control 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Authors. Published under the terms of the CC BY 4.0 license 2017 Abstract The rapidly proliferating cells in plant meristems must be protected from genome damage. Here, we show that the regulatory role of the Arabidopsis RETINOBLASTOMA RELATED (RBR) in cell proliferation can be separated from a novel function in safeguarding genome integrity. Upon DNA damage, RBR and its binding partner E2FA are recruited to heterochromatic γH2AX‐labelled DNA damage foci in an ATM‐ and ATR‐dependent manner. These γH2AX‐labelled DNA lesions are more dispersedly occupied by the conserved repair protein, AtBRCA1, which can also co‐localise with RBR foci. RBR and AtBRCA1 physically interact in vitro and in planta. Genetic interaction between the RBR‐silenced amiRBR and Atbrca1 mutants suggests that RBR and AtBRCA1 may function together in maintaining genome integrity. Together with E2FA, RBR is directly involved in the transcriptional DNA damage response as well as in the cell death pathway that is independent of SOG1, the plant functional analogue of p53. Thus, plant homologs and analogues of major mammalian tumour suppressor proteins form a regulatory network that coordinates cell proliferation with cell and genome integrity. Synopsis Arabidopsis RETINOBLASTOMA RELATED (RBR), the plant homolog of the mammalian retinoblastoma tumor suppressor protein, transcriptionally regulates damage response and cell death pathways, but also directly cooperates with the repair factor BRCA1 to maintain genome integrity after damage. Beyond its role in cell cycle control, RBR has a function in maintaining genome integrity and cell viability.RBR together with E2FA frequently accumulates on γH2AX‐labelled damage foci during DNA damage responses.RBR and AtBRCA1 physically interact and co‐localise on a subset of γH2AX‐labelled nuclear foci.Genetic interactions of RBR and AtBRCA1 support their synergistic action in DNA repair.RBR and E2FA regulate AtBRCA1 transcription and cell death responses in a SOG1‐independent pathway. Graphical Abstract The tumor suppressor plant homolog transcriptionally regulates damage response and cell death pathways, but also directly cooperates with the repair factor BRCA1 to maintain genome integrity after damage. BRCA1 (dpeaa)DE-He213 DNA damage response (dpeaa)DE-He213 E2FA (dpeaa)DE-He213 RETINOBLASTOMA RELATED (dpeaa)DE-He213 Kourova, Hana verfasserin aut Nagy, Szilvia verfasserin aut Nemeth, Edit verfasserin (orcid)0000-0002-9233-0773 aut Magyar, Zoltan verfasserin aut Papdi, Csaba verfasserin (orcid)0000-0003-0640-6098 aut Ahmad, Zaki verfasserin (orcid)0000-0002-0258-704X aut Sanchez‐Perez, Gabino F verfasserin aut Perilli, Serena verfasserin aut Blilou, Ikram verfasserin aut Pettkó‐Szandtner, Aladár verfasserin aut Darula, Zsuzsanna verfasserin aut Meszaros, Tamas verfasserin aut Binarova, Pavla verfasserin aut Bogre, Laszlo verfasserin aut Scheres, Ben verfasserin (orcid)0000-0001-5400-9578 aut Enthalten in The EMBO Journal Nature Publishing Group UK, 2023 36(2017), 9 vom: 20. März, Seite 1261-1278 (DE-627)266022529 (DE-600)1467419-1 1460-2075 nnns volume:36 year:2017 number:9 day:20 month:03 pages:1261-1278 https://dx.doi.org/10.15252/embj.201694561 X:SPRINGER Resolving-System kostenfrei 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_211 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_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_4313 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_4700 AR 36 2017 9 20 03 1261-1278 |
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10.15252/embj.201694561 doi (DE-627)SPR057871922 (SPR)embj.201694561-e DE-627 ger DE-627 rakwb eng Horvath, Beatrix M verfasserin (orcid)0000-0002-6083-992X aut Arabidopsis RETINOBLASTOMA RELATED directly regulates DNA damage responses through functions beyond cell cycle control 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Authors. Published under the terms of the CC BY 4.0 license 2017 Abstract The rapidly proliferating cells in plant meristems must be protected from genome damage. Here, we show that the regulatory role of the Arabidopsis RETINOBLASTOMA RELATED (RBR) in cell proliferation can be separated from a novel function in safeguarding genome integrity. Upon DNA damage, RBR and its binding partner E2FA are recruited to heterochromatic γH2AX‐labelled DNA damage foci in an ATM‐ and ATR‐dependent manner. These γH2AX‐labelled DNA lesions are more dispersedly occupied by the conserved repair protein, AtBRCA1, which can also co‐localise with RBR foci. RBR and AtBRCA1 physically interact in vitro and in planta. Genetic interaction between the RBR‐silenced amiRBR and Atbrca1 mutants suggests that RBR and AtBRCA1 may function together in maintaining genome integrity. Together with E2FA, RBR is directly involved in the transcriptional DNA damage response as well as in the cell death pathway that is independent of SOG1, the plant functional analogue of p53. Thus, plant homologs and analogues of major mammalian tumour suppressor proteins form a regulatory network that coordinates cell proliferation with cell and genome integrity. Synopsis Arabidopsis RETINOBLASTOMA RELATED (RBR), the plant homolog of the mammalian retinoblastoma tumor suppressor protein, transcriptionally regulates damage response and cell death pathways, but also directly cooperates with the repair factor BRCA1 to maintain genome integrity after damage. Beyond its role in cell cycle control, RBR has a function in maintaining genome integrity and cell viability.RBR together with E2FA frequently accumulates on γH2AX‐labelled damage foci during DNA damage responses.RBR and AtBRCA1 physically interact and co‐localise on a subset of γH2AX‐labelled nuclear foci.Genetic interactions of RBR and AtBRCA1 support their synergistic action in DNA repair.RBR and E2FA regulate AtBRCA1 transcription and cell death responses in a SOG1‐independent pathway. Graphical Abstract The tumor suppressor plant homolog transcriptionally regulates damage response and cell death pathways, but also directly cooperates with the repair factor BRCA1 to maintain genome integrity after damage. BRCA1 (dpeaa)DE-He213 DNA damage response (dpeaa)DE-He213 E2FA (dpeaa)DE-He213 RETINOBLASTOMA RELATED (dpeaa)DE-He213 Kourova, Hana verfasserin aut Nagy, Szilvia verfasserin aut Nemeth, Edit verfasserin (orcid)0000-0002-9233-0773 aut Magyar, Zoltan verfasserin aut Papdi, Csaba verfasserin (orcid)0000-0003-0640-6098 aut Ahmad, Zaki verfasserin (orcid)0000-0002-0258-704X aut Sanchez‐Perez, Gabino F verfasserin aut Perilli, Serena verfasserin aut Blilou, Ikram verfasserin aut Pettkó‐Szandtner, Aladár verfasserin aut Darula, Zsuzsanna verfasserin aut Meszaros, Tamas verfasserin aut Binarova, Pavla verfasserin aut Bogre, Laszlo verfasserin aut Scheres, Ben verfasserin (orcid)0000-0001-5400-9578 aut Enthalten in The EMBO Journal Nature Publishing Group UK, 2023 36(2017), 9 vom: 20. März, Seite 1261-1278 (DE-627)266022529 (DE-600)1467419-1 1460-2075 nnns volume:36 year:2017 number:9 day:20 month:03 pages:1261-1278 https://dx.doi.org/10.15252/embj.201694561 X:SPRINGER Resolving-System kostenfrei 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_211 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_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_4313 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_4700 AR 36 2017 9 20 03 1261-1278 |
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10.15252/embj.201694561 doi (DE-627)SPR057871922 (SPR)embj.201694561-e DE-627 ger DE-627 rakwb eng Horvath, Beatrix M verfasserin (orcid)0000-0002-6083-992X aut Arabidopsis RETINOBLASTOMA RELATED directly regulates DNA damage responses through functions beyond cell cycle control 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Authors. Published under the terms of the CC BY 4.0 license 2017 Abstract The rapidly proliferating cells in plant meristems must be protected from genome damage. Here, we show that the regulatory role of the Arabidopsis RETINOBLASTOMA RELATED (RBR) in cell proliferation can be separated from a novel function in safeguarding genome integrity. Upon DNA damage, RBR and its binding partner E2FA are recruited to heterochromatic γH2AX‐labelled DNA damage foci in an ATM‐ and ATR‐dependent manner. These γH2AX‐labelled DNA lesions are more dispersedly occupied by the conserved repair protein, AtBRCA1, which can also co‐localise with RBR foci. RBR and AtBRCA1 physically interact in vitro and in planta. Genetic interaction between the RBR‐silenced amiRBR and Atbrca1 mutants suggests that RBR and AtBRCA1 may function together in maintaining genome integrity. Together with E2FA, RBR is directly involved in the transcriptional DNA damage response as well as in the cell death pathway that is independent of SOG1, the plant functional analogue of p53. Thus, plant homologs and analogues of major mammalian tumour suppressor proteins form a regulatory network that coordinates cell proliferation with cell and genome integrity. Synopsis Arabidopsis RETINOBLASTOMA RELATED (RBR), the plant homolog of the mammalian retinoblastoma tumor suppressor protein, transcriptionally regulates damage response and cell death pathways, but also directly cooperates with the repair factor BRCA1 to maintain genome integrity after damage. Beyond its role in cell cycle control, RBR has a function in maintaining genome integrity and cell viability.RBR together with E2FA frequently accumulates on γH2AX‐labelled damage foci during DNA damage responses.RBR and AtBRCA1 physically interact and co‐localise on a subset of γH2AX‐labelled nuclear foci.Genetic interactions of RBR and AtBRCA1 support their synergistic action in DNA repair.RBR and E2FA regulate AtBRCA1 transcription and cell death responses in a SOG1‐independent pathway. Graphical Abstract The tumor suppressor plant homolog transcriptionally regulates damage response and cell death pathways, but also directly cooperates with the repair factor BRCA1 to maintain genome integrity after damage. BRCA1 (dpeaa)DE-He213 DNA damage response (dpeaa)DE-He213 E2FA (dpeaa)DE-He213 RETINOBLASTOMA RELATED (dpeaa)DE-He213 Kourova, Hana verfasserin aut Nagy, Szilvia verfasserin aut Nemeth, Edit verfasserin (orcid)0000-0002-9233-0773 aut Magyar, Zoltan verfasserin aut Papdi, Csaba verfasserin (orcid)0000-0003-0640-6098 aut Ahmad, Zaki verfasserin (orcid)0000-0002-0258-704X aut Sanchez‐Perez, Gabino F verfasserin aut Perilli, Serena verfasserin aut Blilou, Ikram verfasserin aut Pettkó‐Szandtner, Aladár verfasserin aut Darula, Zsuzsanna verfasserin aut Meszaros, Tamas verfasserin aut Binarova, Pavla verfasserin aut Bogre, Laszlo verfasserin aut Scheres, Ben verfasserin (orcid)0000-0001-5400-9578 aut Enthalten in The EMBO Journal Nature Publishing Group UK, 2023 36(2017), 9 vom: 20. März, Seite 1261-1278 (DE-627)266022529 (DE-600)1467419-1 1460-2075 nnns volume:36 year:2017 number:9 day:20 month:03 pages:1261-1278 https://dx.doi.org/10.15252/embj.201694561 X:SPRINGER Resolving-System kostenfrei 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_211 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_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_4313 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_4700 AR 36 2017 9 20 03 1261-1278 |
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<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000naa a22002652 4500</leader><controlfield tag="001">SPR057871922</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20241018064945.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">241018s2017 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.15252/embj.201694561</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)SPR057871922</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(SPR)embj.201694561-e</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Horvath, Beatrix M</subfield><subfield code="e">verfasserin</subfield><subfield code="0">(orcid)0000-0002-6083-992X</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Arabidopsis RETINOBLASTOMA RELATED directly regulates DNA damage responses through functions beyond cell cycle control</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2017</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="500" ind1=" " ind2=" "><subfield code="a">© The Authors. Published under the terms of the CC BY 4.0 license 2017</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Abstract The rapidly proliferating cells in plant meristems must be protected from genome damage. Here, we show that the regulatory role of the Arabidopsis RETINOBLASTOMA RELATED (RBR) in cell proliferation can be separated from a novel function in safeguarding genome integrity. Upon DNA damage, RBR and its binding partner E2FA are recruited to heterochromatic γH2AX‐labelled DNA damage foci in an ATM‐ and ATR‐dependent manner. These γH2AX‐labelled DNA lesions are more dispersedly occupied by the conserved repair protein, AtBRCA1, which can also co‐localise with RBR foci. RBR and AtBRCA1 physically interact in vitro and in planta. Genetic interaction between the RBR‐silenced amiRBR and Atbrca1 mutants suggests that RBR and AtBRCA1 may function together in maintaining genome integrity. Together with E2FA, RBR is directly involved in the transcriptional DNA damage response as well as in the cell death pathway that is independent of SOG1, the plant functional analogue of p53. Thus, plant homologs and analogues of major mammalian tumour suppressor proteins form a regulatory network that coordinates cell proliferation with cell and genome integrity.</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Synopsis Arabidopsis RETINOBLASTOMA RELATED (RBR), the plant homolog of the mammalian retinoblastoma tumor suppressor protein, transcriptionally regulates damage response and cell death pathways, but also directly cooperates with the repair factor BRCA1 to maintain genome integrity after damage. Beyond its role in cell cycle control, RBR has a function in maintaining genome integrity and cell viability.RBR together with E2FA frequently accumulates on γH2AX‐labelled damage foci during DNA damage responses.RBR and AtBRCA1 physically interact and co‐localise on a subset of γH2AX‐labelled nuclear foci.Genetic interactions of RBR and AtBRCA1 support their synergistic action in DNA repair.RBR and E2FA regulate AtBRCA1 transcription and cell death responses in a SOG1‐independent pathway.</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Graphical Abstract The tumor suppressor plant homolog transcriptionally regulates damage response and cell death pathways, but also directly cooperates with the repair factor BRCA1 to maintain genome integrity after damage.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">BRCA1</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">DNA damage response</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">E2FA</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">RETINOBLASTOMA RELATED</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Kourova, Hana</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Nagy, Szilvia</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Nemeth, Edit</subfield><subfield code="e">verfasserin</subfield><subfield code="0">(orcid)0000-0002-9233-0773</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Magyar, Zoltan</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Papdi, Csaba</subfield><subfield code="e">verfasserin</subfield><subfield code="0">(orcid)0000-0003-0640-6098</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Ahmad, Zaki</subfield><subfield code="e">verfasserin</subfield><subfield code="0">(orcid)0000-0002-0258-704X</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Sanchez‐Perez, Gabino F</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Perilli, Serena</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Blilou, Ikram</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Pettkó‐Szandtner, Aladár</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Darula, Zsuzsanna</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Meszaros, Tamas</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Binarova, Pavla</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Bogre, Laszlo</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Scheres, Ben</subfield><subfield code="e">verfasserin</subfield><subfield code="0">(orcid)0000-0001-5400-9578</subfield><subfield code="4">aut</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="t">The EMBO Journal</subfield><subfield code="d">Nature Publishing Group UK, 2023</subfield><subfield code="g">36(2017), 9 vom: 20. 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|
| author |
Horvath, Beatrix M |
| spellingShingle |
Horvath, Beatrix M misc BRCA1 misc DNA damage response misc E2FA misc RETINOBLASTOMA RELATED Arabidopsis RETINOBLASTOMA RELATED directly regulates DNA damage responses through functions beyond cell cycle control |
| authorStr |
Horvath, Beatrix M |
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@@773@@(DE-627)266022529 |
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electronic Article |
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keep |
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aut aut aut aut aut aut aut aut aut aut aut aut aut aut aut aut |
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springer |
| remote_str |
true |
| illustrated |
Not Illustrated |
| issn |
1460-2075 |
| topic_title |
Arabidopsis RETINOBLASTOMA RELATED directly regulates DNA damage responses through functions beyond cell cycle control BRCA1 (dpeaa)DE-He213 DNA damage response (dpeaa)DE-He213 E2FA (dpeaa)DE-He213 RETINOBLASTOMA RELATED (dpeaa)DE-He213 |
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misc BRCA1 misc DNA damage response misc E2FA misc RETINOBLASTOMA RELATED |
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misc BRCA1 misc DNA damage response misc E2FA misc RETINOBLASTOMA RELATED |
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misc BRCA1 misc DNA damage response misc E2FA misc RETINOBLASTOMA RELATED |
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Elektronische Aufsätze Aufsätze Elektronische Ressource |
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Arabidopsis RETINOBLASTOMA RELATED directly regulates DNA damage responses through functions beyond cell cycle control |
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Arabidopsis RETINOBLASTOMA RELATED directly regulates DNA damage responses through functions beyond cell cycle control |
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Horvath, Beatrix M |
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Horvath, Beatrix M Kourova, Hana Nagy, Szilvia Nemeth, Edit Magyar, Zoltan Papdi, Csaba Ahmad, Zaki Sanchez‐Perez, Gabino F Perilli, Serena Blilou, Ikram Pettkó‐Szandtner, Aladár Darula, Zsuzsanna Meszaros, Tamas Binarova, Pavla Bogre, Laszlo Scheres, Ben |
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arabidopsis retinoblastoma related directly regulates dna damage responses through functions beyond cell cycle control |
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Arabidopsis RETINOBLASTOMA RELATED directly regulates DNA damage responses through functions beyond cell cycle control |
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Abstract The rapidly proliferating cells in plant meristems must be protected from genome damage. Here, we show that the regulatory role of the Arabidopsis RETINOBLASTOMA RELATED (RBR) in cell proliferation can be separated from a novel function in safeguarding genome integrity. Upon DNA damage, RBR and its binding partner E2FA are recruited to heterochromatic γH2AX‐labelled DNA damage foci in an ATM‐ and ATR‐dependent manner. These γH2AX‐labelled DNA lesions are more dispersedly occupied by the conserved repair protein, AtBRCA1, which can also co‐localise with RBR foci. RBR and AtBRCA1 physically interact in vitro and in planta. Genetic interaction between the RBR‐silenced amiRBR and Atbrca1 mutants suggests that RBR and AtBRCA1 may function together in maintaining genome integrity. Together with E2FA, RBR is directly involved in the transcriptional DNA damage response as well as in the cell death pathway that is independent of SOG1, the plant functional analogue of p53. Thus, plant homologs and analogues of major mammalian tumour suppressor proteins form a regulatory network that coordinates cell proliferation with cell and genome integrity. Synopsis Arabidopsis RETINOBLASTOMA RELATED (RBR), the plant homolog of the mammalian retinoblastoma tumor suppressor protein, transcriptionally regulates damage response and cell death pathways, but also directly cooperates with the repair factor BRCA1 to maintain genome integrity after damage. Beyond its role in cell cycle control, RBR has a function in maintaining genome integrity and cell viability.RBR together with E2FA frequently accumulates on γH2AX‐labelled damage foci during DNA damage responses.RBR and AtBRCA1 physically interact and co‐localise on a subset of γH2AX‐labelled nuclear foci.Genetic interactions of RBR and AtBRCA1 support their synergistic action in DNA repair.RBR and E2FA regulate AtBRCA1 transcription and cell death responses in a SOG1‐independent pathway. Graphical Abstract The tumor suppressor plant homolog transcriptionally regulates damage response and cell death pathways, but also directly cooperates with the repair factor BRCA1 to maintain genome integrity after damage. © The Authors. Published under the terms of the CC BY 4.0 license 2017 |
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Abstract The rapidly proliferating cells in plant meristems must be protected from genome damage. Here, we show that the regulatory role of the Arabidopsis RETINOBLASTOMA RELATED (RBR) in cell proliferation can be separated from a novel function in safeguarding genome integrity. Upon DNA damage, RBR and its binding partner E2FA are recruited to heterochromatic γH2AX‐labelled DNA damage foci in an ATM‐ and ATR‐dependent manner. These γH2AX‐labelled DNA lesions are more dispersedly occupied by the conserved repair protein, AtBRCA1, which can also co‐localise with RBR foci. RBR and AtBRCA1 physically interact in vitro and in planta. Genetic interaction between the RBR‐silenced amiRBR and Atbrca1 mutants suggests that RBR and AtBRCA1 may function together in maintaining genome integrity. Together with E2FA, RBR is directly involved in the transcriptional DNA damage response as well as in the cell death pathway that is independent of SOG1, the plant functional analogue of p53. Thus, plant homologs and analogues of major mammalian tumour suppressor proteins form a regulatory network that coordinates cell proliferation with cell and genome integrity. Synopsis Arabidopsis RETINOBLASTOMA RELATED (RBR), the plant homolog of the mammalian retinoblastoma tumor suppressor protein, transcriptionally regulates damage response and cell death pathways, but also directly cooperates with the repair factor BRCA1 to maintain genome integrity after damage. Beyond its role in cell cycle control, RBR has a function in maintaining genome integrity and cell viability.RBR together with E2FA frequently accumulates on γH2AX‐labelled damage foci during DNA damage responses.RBR and AtBRCA1 physically interact and co‐localise on a subset of γH2AX‐labelled nuclear foci.Genetic interactions of RBR and AtBRCA1 support their synergistic action in DNA repair.RBR and E2FA regulate AtBRCA1 transcription and cell death responses in a SOG1‐independent pathway. Graphical Abstract The tumor suppressor plant homolog transcriptionally regulates damage response and cell death pathways, but also directly cooperates with the repair factor BRCA1 to maintain genome integrity after damage. © The Authors. Published under the terms of the CC BY 4.0 license 2017 |
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Abstract The rapidly proliferating cells in plant meristems must be protected from genome damage. Here, we show that the regulatory role of the Arabidopsis RETINOBLASTOMA RELATED (RBR) in cell proliferation can be separated from a novel function in safeguarding genome integrity. Upon DNA damage, RBR and its binding partner E2FA are recruited to heterochromatic γH2AX‐labelled DNA damage foci in an ATM‐ and ATR‐dependent manner. These γH2AX‐labelled DNA lesions are more dispersedly occupied by the conserved repair protein, AtBRCA1, which can also co‐localise with RBR foci. RBR and AtBRCA1 physically interact in vitro and in planta. Genetic interaction between the RBR‐silenced amiRBR and Atbrca1 mutants suggests that RBR and AtBRCA1 may function together in maintaining genome integrity. Together with E2FA, RBR is directly involved in the transcriptional DNA damage response as well as in the cell death pathway that is independent of SOG1, the plant functional analogue of p53. Thus, plant homologs and analogues of major mammalian tumour suppressor proteins form a regulatory network that coordinates cell proliferation with cell and genome integrity. Synopsis Arabidopsis RETINOBLASTOMA RELATED (RBR), the plant homolog of the mammalian retinoblastoma tumor suppressor protein, transcriptionally regulates damage response and cell death pathways, but also directly cooperates with the repair factor BRCA1 to maintain genome integrity after damage. Beyond its role in cell cycle control, RBR has a function in maintaining genome integrity and cell viability.RBR together with E2FA frequently accumulates on γH2AX‐labelled damage foci during DNA damage responses.RBR and AtBRCA1 physically interact and co‐localise on a subset of γH2AX‐labelled nuclear foci.Genetic interactions of RBR and AtBRCA1 support their synergistic action in DNA repair.RBR and E2FA regulate AtBRCA1 transcription and cell death responses in a SOG1‐independent pathway. Graphical Abstract The tumor suppressor plant homolog transcriptionally regulates damage response and cell death pathways, but also directly cooperates with the repair factor BRCA1 to maintain genome integrity after damage. © The Authors. Published under the terms of the CC BY 4.0 license 2017 |
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| score |
7.4009047 |