Arabidopsis E2FA stimulates proliferation and endocycle separately through RBR‐bound and RBR‐free complexes
Abstract Post‐embryonic growth in plants depends on the continuous supply of undifferentiated cells within meristems. Proliferating cells maintain their competence for division by active repression of differentiation and the associated endocycle entry. We show by upregulation and downregulation of E...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Magyar, Zoltán [verfasserIn] Horváth, Beatrix [verfasserIn] Khan, Safina [verfasserIn] Mohammed, Binish [verfasserIn] Henriques, Rossana [verfasserIn] De Veylder, Lieven [verfasserIn] Bakó, László [verfasserIn] Scheres, Ben [verfasserIn] Bögre, László [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2012 |
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| Schlagwörter: |
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| Anmerkung: |
© European Molecular Biology Organization 2012 |
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| Übergeordnetes Werk: |
Enthalten in: The EMBO Journal - Nature Publishing Group UK, 2023, 31(2012), 6 vom: 03. Feb., Seite 1480-1493 |
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| Übergeordnetes Werk: |
volume:31 ; year:2012 ; number:6 ; day:03 ; month:02 ; pages:1480-1493 |
| Links: |
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| DOI / URN: |
10.1038/emboj.2012.13 |
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| Katalog-ID: |
SPR057955743 |
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| 245 | 1 | 0 | |a Arabidopsis E2FA stimulates proliferation and endocycle separately through RBR‐bound and RBR‐free complexes |
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| 520 | |a Abstract Post‐embryonic growth in plants depends on the continuous supply of undifferentiated cells within meristems. Proliferating cells maintain their competence for division by active repression of differentiation and the associated endocycle entry. We show by upregulation and downregulation of E2FA that it is required for maintaining proliferation, as well as for endocycle entry. While E2FB–RBR1 (retinoblastoma‐related protein 1) complexes are reduced after sucrose addition or at elevated CYCD3;1 levels, E2FA maintains a stable complex with RBR1 in proliferating cells. Chromatin immunoprecipitation shows that RBR1 binds in the proximity of E2F promoter elements in CCS52A1 and CSS52A2 genes, central regulators for the switch from proliferation to endocycles. Overexpression of a truncated E2FA mutant ($ E2FA^{ΔRB} $) lacking the RBR1‐binding domain interferes with RBR1 recruitment to promoters through E2FA, leading to decreased meristem size in roots, premature cell expansion and hyperactivated endocycle in leaves. E2F target genes, including CCS52A1 and CCS52A2, are upregulated in $ E2FA^{ΔRB} $ and e2fa knockout lines. These data suggest that E2FA in complex with RBR1 forms a repressor complex in proliferating cells to inhibit premature differentiation and endocycle entry. Thus, E2FA regulates organ growth via two distinct, sequentially operating pathways. | ||
| 520 | |a Abstract The transcription factor E2FA stimulates mutually exclusive plant cell‐cycle states, mitotic proliferation and differentiation‐associated endocycles. In complex with retinoblastoma protein RBR1, E2FA first maintains proliferation by repressing differentiation genes, while later acting independently to promote endocycle entry. | ||
| 650 | 4 | |a cell proliferation |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a endocycle |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a E2F |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a retinoblastoma |7 (dpeaa)DE-He213 | |
| 700 | 1 | |a Horváth, Beatrix |e verfasserin |4 aut | |
| 700 | 1 | |a Khan, Safina |e verfasserin |4 aut | |
| 700 | 1 | |a Mohammed, Binish |e verfasserin |4 aut | |
| 700 | 1 | |a Henriques, Rossana |e verfasserin |4 aut | |
| 700 | 1 | |a De Veylder, Lieven |e verfasserin |4 aut | |
| 700 | 1 | |a Bakó, László |e verfasserin |4 aut | |
| 700 | 1 | |a Scheres, Ben |e verfasserin |4 aut | |
| 700 | 1 | |a Bögre, László |e verfasserin |4 aut | |
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10.1038/emboj.2012.13 doi (DE-627)SPR057955743 (SPR)emboj.2012.13-e DE-627 ger DE-627 rakwb eng Magyar, Zoltán verfasserin aut Arabidopsis E2FA stimulates proliferation and endocycle separately through RBR‐bound and RBR‐free complexes 2012 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © European Molecular Biology Organization 2012 Abstract Post‐embryonic growth in plants depends on the continuous supply of undifferentiated cells within meristems. Proliferating cells maintain their competence for division by active repression of differentiation and the associated endocycle entry. We show by upregulation and downregulation of E2FA that it is required for maintaining proliferation, as well as for endocycle entry. While E2FB–RBR1 (retinoblastoma‐related protein 1) complexes are reduced after sucrose addition or at elevated CYCD3;1 levels, E2FA maintains a stable complex with RBR1 in proliferating cells. Chromatin immunoprecipitation shows that RBR1 binds in the proximity of E2F promoter elements in CCS52A1 and CSS52A2 genes, central regulators for the switch from proliferation to endocycles. Overexpression of a truncated E2FA mutant ($ E2FA^{ΔRB} $) lacking the RBR1‐binding domain interferes with RBR1 recruitment to promoters through E2FA, leading to decreased meristem size in roots, premature cell expansion and hyperactivated endocycle in leaves. E2F target genes, including CCS52A1 and CCS52A2, are upregulated in $ E2FA^{ΔRB} $ and e2fa knockout lines. These data suggest that E2FA in complex with RBR1 forms a repressor complex in proliferating cells to inhibit premature differentiation and endocycle entry. Thus, E2FA regulates organ growth via two distinct, sequentially operating pathways. Abstract The transcription factor E2FA stimulates mutually exclusive plant cell‐cycle states, mitotic proliferation and differentiation‐associated endocycles. In complex with retinoblastoma protein RBR1, E2FA first maintains proliferation by repressing differentiation genes, while later acting independently to promote endocycle entry. cell proliferation (dpeaa)DE-He213 endocycle (dpeaa)DE-He213 E2F (dpeaa)DE-He213 retinoblastoma (dpeaa)DE-He213 Horváth, Beatrix verfasserin aut Khan, Safina verfasserin aut Mohammed, Binish verfasserin aut Henriques, Rossana verfasserin aut De Veylder, Lieven verfasserin aut Bakó, László verfasserin aut Scheres, Ben verfasserin aut Bögre, László verfasserin aut Enthalten in The EMBO Journal Nature Publishing Group UK, 2023 31(2012), 6 vom: 03. Feb., Seite 1480-1493 (DE-627)266022529 (DE-600)1467419-1 1460-2075 nnns volume:31 year:2012 number:6 day:03 month:02 pages:1480-1493 https://dx.doi.org/10.1038/emboj.2012.13 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 31 2012 6 03 02 1480-1493 |
| spelling |
10.1038/emboj.2012.13 doi (DE-627)SPR057955743 (SPR)emboj.2012.13-e DE-627 ger DE-627 rakwb eng Magyar, Zoltán verfasserin aut Arabidopsis E2FA stimulates proliferation and endocycle separately through RBR‐bound and RBR‐free complexes 2012 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © European Molecular Biology Organization 2012 Abstract Post‐embryonic growth in plants depends on the continuous supply of undifferentiated cells within meristems. Proliferating cells maintain their competence for division by active repression of differentiation and the associated endocycle entry. We show by upregulation and downregulation of E2FA that it is required for maintaining proliferation, as well as for endocycle entry. While E2FB–RBR1 (retinoblastoma‐related protein 1) complexes are reduced after sucrose addition or at elevated CYCD3;1 levels, E2FA maintains a stable complex with RBR1 in proliferating cells. Chromatin immunoprecipitation shows that RBR1 binds in the proximity of E2F promoter elements in CCS52A1 and CSS52A2 genes, central regulators for the switch from proliferation to endocycles. Overexpression of a truncated E2FA mutant ($ E2FA^{ΔRB} $) lacking the RBR1‐binding domain interferes with RBR1 recruitment to promoters through E2FA, leading to decreased meristem size in roots, premature cell expansion and hyperactivated endocycle in leaves. E2F target genes, including CCS52A1 and CCS52A2, are upregulated in $ E2FA^{ΔRB} $ and e2fa knockout lines. These data suggest that E2FA in complex with RBR1 forms a repressor complex in proliferating cells to inhibit premature differentiation and endocycle entry. Thus, E2FA regulates organ growth via two distinct, sequentially operating pathways. Abstract The transcription factor E2FA stimulates mutually exclusive plant cell‐cycle states, mitotic proliferation and differentiation‐associated endocycles. In complex with retinoblastoma protein RBR1, E2FA first maintains proliferation by repressing differentiation genes, while later acting independently to promote endocycle entry. cell proliferation (dpeaa)DE-He213 endocycle (dpeaa)DE-He213 E2F (dpeaa)DE-He213 retinoblastoma (dpeaa)DE-He213 Horváth, Beatrix verfasserin aut Khan, Safina verfasserin aut Mohammed, Binish verfasserin aut Henriques, Rossana verfasserin aut De Veylder, Lieven verfasserin aut Bakó, László verfasserin aut Scheres, Ben verfasserin aut Bögre, László verfasserin aut Enthalten in The EMBO Journal Nature Publishing Group UK, 2023 31(2012), 6 vom: 03. Feb., Seite 1480-1493 (DE-627)266022529 (DE-600)1467419-1 1460-2075 nnns volume:31 year:2012 number:6 day:03 month:02 pages:1480-1493 https://dx.doi.org/10.1038/emboj.2012.13 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 31 2012 6 03 02 1480-1493 |
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10.1038/emboj.2012.13 doi (DE-627)SPR057955743 (SPR)emboj.2012.13-e DE-627 ger DE-627 rakwb eng Magyar, Zoltán verfasserin aut Arabidopsis E2FA stimulates proliferation and endocycle separately through RBR‐bound and RBR‐free complexes 2012 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © European Molecular Biology Organization 2012 Abstract Post‐embryonic growth in plants depends on the continuous supply of undifferentiated cells within meristems. Proliferating cells maintain their competence for division by active repression of differentiation and the associated endocycle entry. We show by upregulation and downregulation of E2FA that it is required for maintaining proliferation, as well as for endocycle entry. While E2FB–RBR1 (retinoblastoma‐related protein 1) complexes are reduced after sucrose addition or at elevated CYCD3;1 levels, E2FA maintains a stable complex with RBR1 in proliferating cells. Chromatin immunoprecipitation shows that RBR1 binds in the proximity of E2F promoter elements in CCS52A1 and CSS52A2 genes, central regulators for the switch from proliferation to endocycles. Overexpression of a truncated E2FA mutant ($ E2FA^{ΔRB} $) lacking the RBR1‐binding domain interferes with RBR1 recruitment to promoters through E2FA, leading to decreased meristem size in roots, premature cell expansion and hyperactivated endocycle in leaves. E2F target genes, including CCS52A1 and CCS52A2, are upregulated in $ E2FA^{ΔRB} $ and e2fa knockout lines. These data suggest that E2FA in complex with RBR1 forms a repressor complex in proliferating cells to inhibit premature differentiation and endocycle entry. Thus, E2FA regulates organ growth via two distinct, sequentially operating pathways. Abstract The transcription factor E2FA stimulates mutually exclusive plant cell‐cycle states, mitotic proliferation and differentiation‐associated endocycles. In complex with retinoblastoma protein RBR1, E2FA first maintains proliferation by repressing differentiation genes, while later acting independently to promote endocycle entry. cell proliferation (dpeaa)DE-He213 endocycle (dpeaa)DE-He213 E2F (dpeaa)DE-He213 retinoblastoma (dpeaa)DE-He213 Horváth, Beatrix verfasserin aut Khan, Safina verfasserin aut Mohammed, Binish verfasserin aut Henriques, Rossana verfasserin aut De Veylder, Lieven verfasserin aut Bakó, László verfasserin aut Scheres, Ben verfasserin aut Bögre, László verfasserin aut Enthalten in The EMBO Journal Nature Publishing Group UK, 2023 31(2012), 6 vom: 03. Feb., Seite 1480-1493 (DE-627)266022529 (DE-600)1467419-1 1460-2075 nnns volume:31 year:2012 number:6 day:03 month:02 pages:1480-1493 https://dx.doi.org/10.1038/emboj.2012.13 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 31 2012 6 03 02 1480-1493 |
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10.1038/emboj.2012.13 doi (DE-627)SPR057955743 (SPR)emboj.2012.13-e DE-627 ger DE-627 rakwb eng Magyar, Zoltán verfasserin aut Arabidopsis E2FA stimulates proliferation and endocycle separately through RBR‐bound and RBR‐free complexes 2012 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © European Molecular Biology Organization 2012 Abstract Post‐embryonic growth in plants depends on the continuous supply of undifferentiated cells within meristems. Proliferating cells maintain their competence for division by active repression of differentiation and the associated endocycle entry. We show by upregulation and downregulation of E2FA that it is required for maintaining proliferation, as well as for endocycle entry. While E2FB–RBR1 (retinoblastoma‐related protein 1) complexes are reduced after sucrose addition or at elevated CYCD3;1 levels, E2FA maintains a stable complex with RBR1 in proliferating cells. Chromatin immunoprecipitation shows that RBR1 binds in the proximity of E2F promoter elements in CCS52A1 and CSS52A2 genes, central regulators for the switch from proliferation to endocycles. Overexpression of a truncated E2FA mutant ($ E2FA^{ΔRB} $) lacking the RBR1‐binding domain interferes with RBR1 recruitment to promoters through E2FA, leading to decreased meristem size in roots, premature cell expansion and hyperactivated endocycle in leaves. E2F target genes, including CCS52A1 and CCS52A2, are upregulated in $ E2FA^{ΔRB} $ and e2fa knockout lines. These data suggest that E2FA in complex with RBR1 forms a repressor complex in proliferating cells to inhibit premature differentiation and endocycle entry. Thus, E2FA regulates organ growth via two distinct, sequentially operating pathways. Abstract The transcription factor E2FA stimulates mutually exclusive plant cell‐cycle states, mitotic proliferation and differentiation‐associated endocycles. In complex with retinoblastoma protein RBR1, E2FA first maintains proliferation by repressing differentiation genes, while later acting independently to promote endocycle entry. cell proliferation (dpeaa)DE-He213 endocycle (dpeaa)DE-He213 E2F (dpeaa)DE-He213 retinoblastoma (dpeaa)DE-He213 Horváth, Beatrix verfasserin aut Khan, Safina verfasserin aut Mohammed, Binish verfasserin aut Henriques, Rossana verfasserin aut De Veylder, Lieven verfasserin aut Bakó, László verfasserin aut Scheres, Ben verfasserin aut Bögre, László verfasserin aut Enthalten in The EMBO Journal Nature Publishing Group UK, 2023 31(2012), 6 vom: 03. Feb., Seite 1480-1493 (DE-627)266022529 (DE-600)1467419-1 1460-2075 nnns volume:31 year:2012 number:6 day:03 month:02 pages:1480-1493 https://dx.doi.org/10.1038/emboj.2012.13 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 31 2012 6 03 02 1480-1493 |
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10.1038/emboj.2012.13 doi (DE-627)SPR057955743 (SPR)emboj.2012.13-e DE-627 ger DE-627 rakwb eng Magyar, Zoltán verfasserin aut Arabidopsis E2FA stimulates proliferation and endocycle separately through RBR‐bound and RBR‐free complexes 2012 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © European Molecular Biology Organization 2012 Abstract Post‐embryonic growth in plants depends on the continuous supply of undifferentiated cells within meristems. Proliferating cells maintain their competence for division by active repression of differentiation and the associated endocycle entry. We show by upregulation and downregulation of E2FA that it is required for maintaining proliferation, as well as for endocycle entry. While E2FB–RBR1 (retinoblastoma‐related protein 1) complexes are reduced after sucrose addition or at elevated CYCD3;1 levels, E2FA maintains a stable complex with RBR1 in proliferating cells. Chromatin immunoprecipitation shows that RBR1 binds in the proximity of E2F promoter elements in CCS52A1 and CSS52A2 genes, central regulators for the switch from proliferation to endocycles. Overexpression of a truncated E2FA mutant ($ E2FA^{ΔRB} $) lacking the RBR1‐binding domain interferes with RBR1 recruitment to promoters through E2FA, leading to decreased meristem size in roots, premature cell expansion and hyperactivated endocycle in leaves. E2F target genes, including CCS52A1 and CCS52A2, are upregulated in $ E2FA^{ΔRB} $ and e2fa knockout lines. These data suggest that E2FA in complex with RBR1 forms a repressor complex in proliferating cells to inhibit premature differentiation and endocycle entry. Thus, E2FA regulates organ growth via two distinct, sequentially operating pathways. Abstract The transcription factor E2FA stimulates mutually exclusive plant cell‐cycle states, mitotic proliferation and differentiation‐associated endocycles. In complex with retinoblastoma protein RBR1, E2FA first maintains proliferation by repressing differentiation genes, while later acting independently to promote endocycle entry. cell proliferation (dpeaa)DE-He213 endocycle (dpeaa)DE-He213 E2F (dpeaa)DE-He213 retinoblastoma (dpeaa)DE-He213 Horváth, Beatrix verfasserin aut Khan, Safina verfasserin aut Mohammed, Binish verfasserin aut Henriques, Rossana verfasserin aut De Veylder, Lieven verfasserin aut Bakó, László verfasserin aut Scheres, Ben verfasserin aut Bögre, László verfasserin aut Enthalten in The EMBO Journal Nature Publishing Group UK, 2023 31(2012), 6 vom: 03. Feb., Seite 1480-1493 (DE-627)266022529 (DE-600)1467419-1 1460-2075 nnns volume:31 year:2012 number:6 day:03 month:02 pages:1480-1493 https://dx.doi.org/10.1038/emboj.2012.13 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 31 2012 6 03 02 1480-1493 |
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Enthalten in The EMBO Journal 31(2012), 6 vom: 03. Feb., Seite 1480-1493 volume:31 year:2012 number:6 day:03 month:02 pages:1480-1493 |
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Magyar, Zoltán @@aut@@ Horváth, Beatrix @@aut@@ Khan, Safina @@aut@@ Mohammed, Binish @@aut@@ Henriques, Rossana @@aut@@ De Veylder, Lieven @@aut@@ Bakó, László @@aut@@ Scheres, Ben @@aut@@ Bögre, László @@aut@@ |
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E2F target genes, including CCS52A1 and CCS52A2, are upregulated in $ E2FA^{ΔRB} $ and e2fa knockout lines. These data suggest that E2FA in complex with RBR1 forms a repressor complex in proliferating cells to inhibit premature differentiation and endocycle entry. Thus, E2FA regulates organ growth via two distinct, sequentially operating pathways.</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Abstract The transcription factor E2FA stimulates mutually exclusive plant cell‐cycle states, mitotic proliferation and differentiation‐associated endocycles. 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Magyar, Zoltán |
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Magyar, Zoltán misc cell proliferation misc endocycle misc E2F misc retinoblastoma Arabidopsis E2FA stimulates proliferation and endocycle separately through RBR‐bound and RBR‐free complexes |
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Magyar, Zoltán |
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Arabidopsis E2FA stimulates proliferation and endocycle separately through RBR‐bound and RBR‐free complexes cell proliferation (dpeaa)DE-He213 endocycle (dpeaa)DE-He213 E2F (dpeaa)DE-He213 retinoblastoma (dpeaa)DE-He213 |
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misc cell proliferation misc endocycle misc E2F misc retinoblastoma |
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misc cell proliferation misc endocycle misc E2F misc retinoblastoma |
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misc cell proliferation misc endocycle misc E2F misc retinoblastoma |
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Elektronische Aufsätze Aufsätze Elektronische Ressource |
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Arabidopsis E2FA stimulates proliferation and endocycle separately through RBR‐bound and RBR‐free complexes |
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(DE-627)SPR057955743 (SPR)emboj.2012.13-e |
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Arabidopsis E2FA stimulates proliferation and endocycle separately through RBR‐bound and RBR‐free complexes |
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Magyar, Zoltán |
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Magyar, Zoltán Horváth, Beatrix Khan, Safina Mohammed, Binish Henriques, Rossana De Veylder, Lieven Bakó, László Scheres, Ben Bögre, László |
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Magyar, Zoltán |
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10.1038/emboj.2012.13 |
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arabidopsis e2fa stimulates proliferation and endocycle separately through rbr‐bound and rbr‐free complexes |
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Arabidopsis E2FA stimulates proliferation and endocycle separately through RBR‐bound and RBR‐free complexes |
| abstract |
Abstract Post‐embryonic growth in plants depends on the continuous supply of undifferentiated cells within meristems. Proliferating cells maintain their competence for division by active repression of differentiation and the associated endocycle entry. We show by upregulation and downregulation of E2FA that it is required for maintaining proliferation, as well as for endocycle entry. While E2FB–RBR1 (retinoblastoma‐related protein 1) complexes are reduced after sucrose addition or at elevated CYCD3;1 levels, E2FA maintains a stable complex with RBR1 in proliferating cells. Chromatin immunoprecipitation shows that RBR1 binds in the proximity of E2F promoter elements in CCS52A1 and CSS52A2 genes, central regulators for the switch from proliferation to endocycles. Overexpression of a truncated E2FA mutant ($ E2FA^{ΔRB} $) lacking the RBR1‐binding domain interferes with RBR1 recruitment to promoters through E2FA, leading to decreased meristem size in roots, premature cell expansion and hyperactivated endocycle in leaves. E2F target genes, including CCS52A1 and CCS52A2, are upregulated in $ E2FA^{ΔRB} $ and e2fa knockout lines. These data suggest that E2FA in complex with RBR1 forms a repressor complex in proliferating cells to inhibit premature differentiation and endocycle entry. Thus, E2FA regulates organ growth via two distinct, sequentially operating pathways. Abstract The transcription factor E2FA stimulates mutually exclusive plant cell‐cycle states, mitotic proliferation and differentiation‐associated endocycles. In complex with retinoblastoma protein RBR1, E2FA first maintains proliferation by repressing differentiation genes, while later acting independently to promote endocycle entry. © European Molecular Biology Organization 2012 |
| abstractGer |
Abstract Post‐embryonic growth in plants depends on the continuous supply of undifferentiated cells within meristems. Proliferating cells maintain their competence for division by active repression of differentiation and the associated endocycle entry. We show by upregulation and downregulation of E2FA that it is required for maintaining proliferation, as well as for endocycle entry. While E2FB–RBR1 (retinoblastoma‐related protein 1) complexes are reduced after sucrose addition or at elevated CYCD3;1 levels, E2FA maintains a stable complex with RBR1 in proliferating cells. Chromatin immunoprecipitation shows that RBR1 binds in the proximity of E2F promoter elements in CCS52A1 and CSS52A2 genes, central regulators for the switch from proliferation to endocycles. Overexpression of a truncated E2FA mutant ($ E2FA^{ΔRB} $) lacking the RBR1‐binding domain interferes with RBR1 recruitment to promoters through E2FA, leading to decreased meristem size in roots, premature cell expansion and hyperactivated endocycle in leaves. E2F target genes, including CCS52A1 and CCS52A2, are upregulated in $ E2FA^{ΔRB} $ and e2fa knockout lines. These data suggest that E2FA in complex with RBR1 forms a repressor complex in proliferating cells to inhibit premature differentiation and endocycle entry. Thus, E2FA regulates organ growth via two distinct, sequentially operating pathways. Abstract The transcription factor E2FA stimulates mutually exclusive plant cell‐cycle states, mitotic proliferation and differentiation‐associated endocycles. In complex with retinoblastoma protein RBR1, E2FA first maintains proliferation by repressing differentiation genes, while later acting independently to promote endocycle entry. © European Molecular Biology Organization 2012 |
| abstract_unstemmed |
Abstract Post‐embryonic growth in plants depends on the continuous supply of undifferentiated cells within meristems. Proliferating cells maintain their competence for division by active repression of differentiation and the associated endocycle entry. We show by upregulation and downregulation of E2FA that it is required for maintaining proliferation, as well as for endocycle entry. While E2FB–RBR1 (retinoblastoma‐related protein 1) complexes are reduced after sucrose addition or at elevated CYCD3;1 levels, E2FA maintains a stable complex with RBR1 in proliferating cells. Chromatin immunoprecipitation shows that RBR1 binds in the proximity of E2F promoter elements in CCS52A1 and CSS52A2 genes, central regulators for the switch from proliferation to endocycles. Overexpression of a truncated E2FA mutant ($ E2FA^{ΔRB} $) lacking the RBR1‐binding domain interferes with RBR1 recruitment to promoters through E2FA, leading to decreased meristem size in roots, premature cell expansion and hyperactivated endocycle in leaves. E2F target genes, including CCS52A1 and CCS52A2, are upregulated in $ E2FA^{ΔRB} $ and e2fa knockout lines. These data suggest that E2FA in complex with RBR1 forms a repressor complex in proliferating cells to inhibit premature differentiation and endocycle entry. Thus, E2FA regulates organ growth via two distinct, sequentially operating pathways. Abstract The transcription factor E2FA stimulates mutually exclusive plant cell‐cycle states, mitotic proliferation and differentiation‐associated endocycles. In complex with retinoblastoma protein RBR1, E2FA first maintains proliferation by repressing differentiation genes, while later acting independently to promote endocycle entry. © European Molecular Biology Organization 2012 |
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| title_short |
Arabidopsis E2FA stimulates proliferation and endocycle separately through RBR‐bound and RBR‐free complexes |
| url |
https://dx.doi.org/10.1038/emboj.2012.13 |
| remote_bool |
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| author2 |
Horváth, Beatrix Khan, Safina Mohammed, Binish Henriques, Rossana De Veylder, Lieven Bakó, László Scheres, Ben Bögre, László |
| author2Str |
Horváth, Beatrix Khan, Safina Mohammed, Binish Henriques, Rossana De Veylder, Lieven Bakó, László Scheres, Ben Bögre, László |
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| doi_str |
10.1038/emboj.2012.13 |
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2024-10-22T04:52:04.904Z |
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| score |
7.3985834 |