Functions of eIF3 downstream of 48S assembly impact AUG recognition and GCN4 translational control
Abstract The binding of eIF2–GTP–$ tRNA_{i} $Met ternary complex (TC) to 40S subunits is impaired in yeast prt1‐1 (eIF3b) mutant extracts, but evidence is lacking that TC recruitment is a critical function of eIF3 in vivo. If TC binding was rate‐limiting in prt1‐1 cells, overexpressing TC should sup...
Ausführliche Beschreibung
Autor*in: |
Nielsen, Klaus H [verfasserIn] Szamecz, Béla [verfasserIn] Valášek, Leoš [verfasserIn] Jivotovskaya, Antonina [verfasserIn] Shin, Byung‐Sik [verfasserIn] Hinnebusch, Alan G [verfasserIn] |
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E-Artikel |
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Sprache: |
Englisch |
Erschienen: |
2004 |
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Schlagwörter: |
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Anmerkung: |
© European Molecular Biology Organization 2004 |
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Übergeordnetes Werk: |
Enthalten in: The EMBO Journal - Nature Publishing Group UK, 2023, 23(2004), 5 vom: 19. Feb., Seite 1166-1177 |
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Übergeordnetes Werk: |
volume:23 ; year:2004 ; number:5 ; day:19 ; month:02 ; pages:1166-1177 |
Links: |
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DOI / URN: |
10.1038/sj.emboj.7600116 |
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Katalog-ID: |
SPR057923485 |
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100 | 1 | |a Nielsen, Klaus H |e verfasserin |4 aut | |
245 | 1 | 0 | |a Functions of eIF3 downstream of 48S assembly impact AUG recognition and GCN4 translational control |
264 | 1 | |c 2004 | |
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520 | |a Abstract The binding of eIF2–GTP–$ tRNA_{i} $Met ternary complex (TC) to 40S subunits is impaired in yeast prt1‐1 (eIF3b) mutant extracts, but evidence is lacking that TC recruitment is a critical function of eIF3 in vivo. If TC binding was rate‐limiting in prt1‐1 cells, overexpressing TC should suppress the temperature‐sensitive phenotype and GCN4 translation should be strongly derepressed in this mutant, but neither was observed. Rather, GCN4 translation is noninducible in prt1‐1 cells, and genetic analysis indicates defective ribosomal scanning between the upstream open reading frames that mediate translational control. prt1‐1 cells also show reduced utilization of a near‐cognate start codon, implicating eIF3 in AUG selection. Using in vivo cross‐linking, we observed accumulation of TC and mRNA/eIF4G on 40S subunits and a 48S ‘halfmer’ in prt1‐1 cells. Genetic evidence suggests that 40S–60S subunit joining is not rate‐limiting in the prt1‐1 mutant. Thus, eIF3b functions between 48S assembly and subunit joining to influence AUG recognition and reinitiation on GCN4 mRNA. Other mutations that disrupt eIF2–eIF3 contacts in the multifactor complex (MFC) diminished 40S‐bound TC, indicating that MFC formation enhances 43S assembly in vivo. | ||
650 | 4 | |a eIF3 |7 (dpeaa)DE-He213 | |
650 | 4 | |a GCN4 translational control |7 (dpeaa)DE-He213 | |
650 | 4 | |a multifactor complex (MFC) |7 (dpeaa)DE-He213 | |
650 | 4 | |a PRT1 |7 (dpeaa)DE-He213 | |
650 | 4 | |a yeast |7 (dpeaa)DE-He213 | |
700 | 1 | |a Szamecz, Béla |e verfasserin |4 aut | |
700 | 1 | |a Valášek, Leoš |e verfasserin |4 aut | |
700 | 1 | |a Jivotovskaya, Antonina |e verfasserin |4 aut | |
700 | 1 | |a Shin, Byung‐Sik |e verfasserin |4 aut | |
700 | 1 | |a Hinnebusch, Alan G |e verfasserin |4 aut | |
773 | 0 | 8 | |i Enthalten in |t The EMBO Journal |d Nature Publishing Group UK, 2023 |g 23(2004), 5 vom: 19. Feb., Seite 1166-1177 |w (DE-627)266022529 |w (DE-600)1467419-1 |x 1460-2075 |7 nnns |
773 | 1 | 8 | |g volume:23 |g year:2004 |g number:5 |g day:19 |g month:02 |g pages:1166-1177 |
856 | 4 | 0 | |u https://dx.doi.org/10.1038/sj.emboj.7600116 |m X:SPRINGER |x Resolving-System |z lizenzpflichtig |3 Volltext |
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912 | |a GBV_ILN_2057 | ||
912 | |a GBV_ILN_2059 | ||
912 | |a GBV_ILN_2061 | ||
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912 | |a GBV_ILN_2118 | ||
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912 | |a GBV_ILN_2470 | ||
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912 | |a GBV_ILN_2507 | ||
912 | |a GBV_ILN_2522 | ||
912 | |a GBV_ILN_2548 | ||
912 | |a GBV_ILN_4012 | ||
912 | |a GBV_ILN_4029 | ||
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912 | |a GBV_ILN_4037 | ||
912 | |a GBV_ILN_4046 | ||
912 | |a GBV_ILN_4112 | ||
912 | |a GBV_ILN_4116 | ||
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912 | |a GBV_ILN_4322 | ||
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912 | |a GBV_ILN_4328 | ||
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912 | |a GBV_ILN_4598 | ||
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2004 |
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10.1038/sj.emboj.7600116 doi (DE-627)SPR057923485 (SPR)sj.emboj.7600116-e DE-627 ger DE-627 rakwb eng Nielsen, Klaus H verfasserin aut Functions of eIF3 downstream of 48S assembly impact AUG recognition and GCN4 translational control 2004 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © European Molecular Biology Organization 2004 Abstract The binding of eIF2–GTP–$ tRNA_{i} $Met ternary complex (TC) to 40S subunits is impaired in yeast prt1‐1 (eIF3b) mutant extracts, but evidence is lacking that TC recruitment is a critical function of eIF3 in vivo. If TC binding was rate‐limiting in prt1‐1 cells, overexpressing TC should suppress the temperature‐sensitive phenotype and GCN4 translation should be strongly derepressed in this mutant, but neither was observed. Rather, GCN4 translation is noninducible in prt1‐1 cells, and genetic analysis indicates defective ribosomal scanning between the upstream open reading frames that mediate translational control. prt1‐1 cells also show reduced utilization of a near‐cognate start codon, implicating eIF3 in AUG selection. Using in vivo cross‐linking, we observed accumulation of TC and mRNA/eIF4G on 40S subunits and a 48S ‘halfmer’ in prt1‐1 cells. Genetic evidence suggests that 40S–60S subunit joining is not rate‐limiting in the prt1‐1 mutant. Thus, eIF3b functions between 48S assembly and subunit joining to influence AUG recognition and reinitiation on GCN4 mRNA. Other mutations that disrupt eIF2–eIF3 contacts in the multifactor complex (MFC) diminished 40S‐bound TC, indicating that MFC formation enhances 43S assembly in vivo. eIF3 (dpeaa)DE-He213 GCN4 translational control (dpeaa)DE-He213 multifactor complex (MFC) (dpeaa)DE-He213 PRT1 (dpeaa)DE-He213 yeast (dpeaa)DE-He213 Szamecz, Béla verfasserin aut Valášek, Leoš verfasserin aut Jivotovskaya, Antonina verfasserin aut Shin, Byung‐Sik verfasserin aut Hinnebusch, Alan G verfasserin aut Enthalten in The EMBO Journal Nature Publishing Group UK, 2023 23(2004), 5 vom: 19. Feb., Seite 1166-1177 (DE-627)266022529 (DE-600)1467419-1 1460-2075 nnns volume:23 year:2004 number:5 day:19 month:02 pages:1166-1177 https://dx.doi.org/10.1038/sj.emboj.7600116 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 23 2004 5 19 02 1166-1177 |
spelling |
10.1038/sj.emboj.7600116 doi (DE-627)SPR057923485 (SPR)sj.emboj.7600116-e DE-627 ger DE-627 rakwb eng Nielsen, Klaus H verfasserin aut Functions of eIF3 downstream of 48S assembly impact AUG recognition and GCN4 translational control 2004 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © European Molecular Biology Organization 2004 Abstract The binding of eIF2–GTP–$ tRNA_{i} $Met ternary complex (TC) to 40S subunits is impaired in yeast prt1‐1 (eIF3b) mutant extracts, but evidence is lacking that TC recruitment is a critical function of eIF3 in vivo. If TC binding was rate‐limiting in prt1‐1 cells, overexpressing TC should suppress the temperature‐sensitive phenotype and GCN4 translation should be strongly derepressed in this mutant, but neither was observed. Rather, GCN4 translation is noninducible in prt1‐1 cells, and genetic analysis indicates defective ribosomal scanning between the upstream open reading frames that mediate translational control. prt1‐1 cells also show reduced utilization of a near‐cognate start codon, implicating eIF3 in AUG selection. Using in vivo cross‐linking, we observed accumulation of TC and mRNA/eIF4G on 40S subunits and a 48S ‘halfmer’ in prt1‐1 cells. Genetic evidence suggests that 40S–60S subunit joining is not rate‐limiting in the prt1‐1 mutant. Thus, eIF3b functions between 48S assembly and subunit joining to influence AUG recognition and reinitiation on GCN4 mRNA. Other mutations that disrupt eIF2–eIF3 contacts in the multifactor complex (MFC) diminished 40S‐bound TC, indicating that MFC formation enhances 43S assembly in vivo. eIF3 (dpeaa)DE-He213 GCN4 translational control (dpeaa)DE-He213 multifactor complex (MFC) (dpeaa)DE-He213 PRT1 (dpeaa)DE-He213 yeast (dpeaa)DE-He213 Szamecz, Béla verfasserin aut Valášek, Leoš verfasserin aut Jivotovskaya, Antonina verfasserin aut Shin, Byung‐Sik verfasserin aut Hinnebusch, Alan G verfasserin aut Enthalten in The EMBO Journal Nature Publishing Group UK, 2023 23(2004), 5 vom: 19. Feb., Seite 1166-1177 (DE-627)266022529 (DE-600)1467419-1 1460-2075 nnns volume:23 year:2004 number:5 day:19 month:02 pages:1166-1177 https://dx.doi.org/10.1038/sj.emboj.7600116 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 23 2004 5 19 02 1166-1177 |
allfields_unstemmed |
10.1038/sj.emboj.7600116 doi (DE-627)SPR057923485 (SPR)sj.emboj.7600116-e DE-627 ger DE-627 rakwb eng Nielsen, Klaus H verfasserin aut Functions of eIF3 downstream of 48S assembly impact AUG recognition and GCN4 translational control 2004 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © European Molecular Biology Organization 2004 Abstract The binding of eIF2–GTP–$ tRNA_{i} $Met ternary complex (TC) to 40S subunits is impaired in yeast prt1‐1 (eIF3b) mutant extracts, but evidence is lacking that TC recruitment is a critical function of eIF3 in vivo. If TC binding was rate‐limiting in prt1‐1 cells, overexpressing TC should suppress the temperature‐sensitive phenotype and GCN4 translation should be strongly derepressed in this mutant, but neither was observed. Rather, GCN4 translation is noninducible in prt1‐1 cells, and genetic analysis indicates defective ribosomal scanning between the upstream open reading frames that mediate translational control. prt1‐1 cells also show reduced utilization of a near‐cognate start codon, implicating eIF3 in AUG selection. Using in vivo cross‐linking, we observed accumulation of TC and mRNA/eIF4G on 40S subunits and a 48S ‘halfmer’ in prt1‐1 cells. Genetic evidence suggests that 40S–60S subunit joining is not rate‐limiting in the prt1‐1 mutant. Thus, eIF3b functions between 48S assembly and subunit joining to influence AUG recognition and reinitiation on GCN4 mRNA. Other mutations that disrupt eIF2–eIF3 contacts in the multifactor complex (MFC) diminished 40S‐bound TC, indicating that MFC formation enhances 43S assembly in vivo. eIF3 (dpeaa)DE-He213 GCN4 translational control (dpeaa)DE-He213 multifactor complex (MFC) (dpeaa)DE-He213 PRT1 (dpeaa)DE-He213 yeast (dpeaa)DE-He213 Szamecz, Béla verfasserin aut Valášek, Leoš verfasserin aut Jivotovskaya, Antonina verfasserin aut Shin, Byung‐Sik verfasserin aut Hinnebusch, Alan G verfasserin aut Enthalten in The EMBO Journal Nature Publishing Group UK, 2023 23(2004), 5 vom: 19. Feb., Seite 1166-1177 (DE-627)266022529 (DE-600)1467419-1 1460-2075 nnns volume:23 year:2004 number:5 day:19 month:02 pages:1166-1177 https://dx.doi.org/10.1038/sj.emboj.7600116 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 23 2004 5 19 02 1166-1177 |
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10.1038/sj.emboj.7600116 doi (DE-627)SPR057923485 (SPR)sj.emboj.7600116-e DE-627 ger DE-627 rakwb eng Nielsen, Klaus H verfasserin aut Functions of eIF3 downstream of 48S assembly impact AUG recognition and GCN4 translational control 2004 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © European Molecular Biology Organization 2004 Abstract The binding of eIF2–GTP–$ tRNA_{i} $Met ternary complex (TC) to 40S subunits is impaired in yeast prt1‐1 (eIF3b) mutant extracts, but evidence is lacking that TC recruitment is a critical function of eIF3 in vivo. If TC binding was rate‐limiting in prt1‐1 cells, overexpressing TC should suppress the temperature‐sensitive phenotype and GCN4 translation should be strongly derepressed in this mutant, but neither was observed. Rather, GCN4 translation is noninducible in prt1‐1 cells, and genetic analysis indicates defective ribosomal scanning between the upstream open reading frames that mediate translational control. prt1‐1 cells also show reduced utilization of a near‐cognate start codon, implicating eIF3 in AUG selection. Using in vivo cross‐linking, we observed accumulation of TC and mRNA/eIF4G on 40S subunits and a 48S ‘halfmer’ in prt1‐1 cells. Genetic evidence suggests that 40S–60S subunit joining is not rate‐limiting in the prt1‐1 mutant. Thus, eIF3b functions between 48S assembly and subunit joining to influence AUG recognition and reinitiation on GCN4 mRNA. Other mutations that disrupt eIF2–eIF3 contacts in the multifactor complex (MFC) diminished 40S‐bound TC, indicating that MFC formation enhances 43S assembly in vivo. eIF3 (dpeaa)DE-He213 GCN4 translational control (dpeaa)DE-He213 multifactor complex (MFC) (dpeaa)DE-He213 PRT1 (dpeaa)DE-He213 yeast (dpeaa)DE-He213 Szamecz, Béla verfasserin aut Valášek, Leoš verfasserin aut Jivotovskaya, Antonina verfasserin aut Shin, Byung‐Sik verfasserin aut Hinnebusch, Alan G verfasserin aut Enthalten in The EMBO Journal Nature Publishing Group UK, 2023 23(2004), 5 vom: 19. Feb., Seite 1166-1177 (DE-627)266022529 (DE-600)1467419-1 1460-2075 nnns volume:23 year:2004 number:5 day:19 month:02 pages:1166-1177 https://dx.doi.org/10.1038/sj.emboj.7600116 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 23 2004 5 19 02 1166-1177 |
allfieldsSound |
10.1038/sj.emboj.7600116 doi (DE-627)SPR057923485 (SPR)sj.emboj.7600116-e DE-627 ger DE-627 rakwb eng Nielsen, Klaus H verfasserin aut Functions of eIF3 downstream of 48S assembly impact AUG recognition and GCN4 translational control 2004 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © European Molecular Biology Organization 2004 Abstract The binding of eIF2–GTP–$ tRNA_{i} $Met ternary complex (TC) to 40S subunits is impaired in yeast prt1‐1 (eIF3b) mutant extracts, but evidence is lacking that TC recruitment is a critical function of eIF3 in vivo. If TC binding was rate‐limiting in prt1‐1 cells, overexpressing TC should suppress the temperature‐sensitive phenotype and GCN4 translation should be strongly derepressed in this mutant, but neither was observed. Rather, GCN4 translation is noninducible in prt1‐1 cells, and genetic analysis indicates defective ribosomal scanning between the upstream open reading frames that mediate translational control. prt1‐1 cells also show reduced utilization of a near‐cognate start codon, implicating eIF3 in AUG selection. Using in vivo cross‐linking, we observed accumulation of TC and mRNA/eIF4G on 40S subunits and a 48S ‘halfmer’ in prt1‐1 cells. Genetic evidence suggests that 40S–60S subunit joining is not rate‐limiting in the prt1‐1 mutant. Thus, eIF3b functions between 48S assembly and subunit joining to influence AUG recognition and reinitiation on GCN4 mRNA. Other mutations that disrupt eIF2–eIF3 contacts in the multifactor complex (MFC) diminished 40S‐bound TC, indicating that MFC formation enhances 43S assembly in vivo. eIF3 (dpeaa)DE-He213 GCN4 translational control (dpeaa)DE-He213 multifactor complex (MFC) (dpeaa)DE-He213 PRT1 (dpeaa)DE-He213 yeast (dpeaa)DE-He213 Szamecz, Béla verfasserin aut Valášek, Leoš verfasserin aut Jivotovskaya, Antonina verfasserin aut Shin, Byung‐Sik verfasserin aut Hinnebusch, Alan G verfasserin aut Enthalten in The EMBO Journal Nature Publishing Group UK, 2023 23(2004), 5 vom: 19. Feb., Seite 1166-1177 (DE-627)266022529 (DE-600)1467419-1 1460-2075 nnns volume:23 year:2004 number:5 day:19 month:02 pages:1166-1177 https://dx.doi.org/10.1038/sj.emboj.7600116 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 23 2004 5 19 02 1166-1177 |
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Enthalten in The EMBO Journal 23(2004), 5 vom: 19. Feb., Seite 1166-1177 volume:23 year:2004 number:5 day:19 month:02 pages:1166-1177 |
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Nielsen, Klaus H @@aut@@ Szamecz, Béla @@aut@@ Valášek, Leoš @@aut@@ Jivotovskaya, Antonina @@aut@@ Shin, Byung‐Sik @@aut@@ Hinnebusch, Alan G @@aut@@ |
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Nielsen, Klaus H |
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Nielsen, Klaus H misc eIF3 misc GCN4 translational control misc multifactor complex (MFC) misc PRT1 misc yeast Functions of eIF3 downstream of 48S assembly impact AUG recognition and GCN4 translational control |
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Functions of eIF3 downstream of 48S assembly impact AUG recognition and GCN4 translational control eIF3 (dpeaa)DE-He213 GCN4 translational control (dpeaa)DE-He213 multifactor complex (MFC) (dpeaa)DE-He213 PRT1 (dpeaa)DE-He213 yeast (dpeaa)DE-He213 |
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misc eIF3 misc GCN4 translational control misc multifactor complex (MFC) misc PRT1 misc yeast |
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Functions of eIF3 downstream of 48S assembly impact AUG recognition and GCN4 translational control |
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functions of eif3 downstream of 48s assembly impact aug recognition and gcn4 translational control |
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Functions of eIF3 downstream of 48S assembly impact AUG recognition and GCN4 translational control |
abstract |
Abstract The binding of eIF2–GTP–$ tRNA_{i} $Met ternary complex (TC) to 40S subunits is impaired in yeast prt1‐1 (eIF3b) mutant extracts, but evidence is lacking that TC recruitment is a critical function of eIF3 in vivo. If TC binding was rate‐limiting in prt1‐1 cells, overexpressing TC should suppress the temperature‐sensitive phenotype and GCN4 translation should be strongly derepressed in this mutant, but neither was observed. Rather, GCN4 translation is noninducible in prt1‐1 cells, and genetic analysis indicates defective ribosomal scanning between the upstream open reading frames that mediate translational control. prt1‐1 cells also show reduced utilization of a near‐cognate start codon, implicating eIF3 in AUG selection. Using in vivo cross‐linking, we observed accumulation of TC and mRNA/eIF4G on 40S subunits and a 48S ‘halfmer’ in prt1‐1 cells. Genetic evidence suggests that 40S–60S subunit joining is not rate‐limiting in the prt1‐1 mutant. Thus, eIF3b functions between 48S assembly and subunit joining to influence AUG recognition and reinitiation on GCN4 mRNA. Other mutations that disrupt eIF2–eIF3 contacts in the multifactor complex (MFC) diminished 40S‐bound TC, indicating that MFC formation enhances 43S assembly in vivo. © European Molecular Biology Organization 2004 |
abstractGer |
Abstract The binding of eIF2–GTP–$ tRNA_{i} $Met ternary complex (TC) to 40S subunits is impaired in yeast prt1‐1 (eIF3b) mutant extracts, but evidence is lacking that TC recruitment is a critical function of eIF3 in vivo. If TC binding was rate‐limiting in prt1‐1 cells, overexpressing TC should suppress the temperature‐sensitive phenotype and GCN4 translation should be strongly derepressed in this mutant, but neither was observed. Rather, GCN4 translation is noninducible in prt1‐1 cells, and genetic analysis indicates defective ribosomal scanning between the upstream open reading frames that mediate translational control. prt1‐1 cells also show reduced utilization of a near‐cognate start codon, implicating eIF3 in AUG selection. Using in vivo cross‐linking, we observed accumulation of TC and mRNA/eIF4G on 40S subunits and a 48S ‘halfmer’ in prt1‐1 cells. Genetic evidence suggests that 40S–60S subunit joining is not rate‐limiting in the prt1‐1 mutant. Thus, eIF3b functions between 48S assembly and subunit joining to influence AUG recognition and reinitiation on GCN4 mRNA. Other mutations that disrupt eIF2–eIF3 contacts in the multifactor complex (MFC) diminished 40S‐bound TC, indicating that MFC formation enhances 43S assembly in vivo. © European Molecular Biology Organization 2004 |
abstract_unstemmed |
Abstract The binding of eIF2–GTP–$ tRNA_{i} $Met ternary complex (TC) to 40S subunits is impaired in yeast prt1‐1 (eIF3b) mutant extracts, but evidence is lacking that TC recruitment is a critical function of eIF3 in vivo. If TC binding was rate‐limiting in prt1‐1 cells, overexpressing TC should suppress the temperature‐sensitive phenotype and GCN4 translation should be strongly derepressed in this mutant, but neither was observed. Rather, GCN4 translation is noninducible in prt1‐1 cells, and genetic analysis indicates defective ribosomal scanning between the upstream open reading frames that mediate translational control. prt1‐1 cells also show reduced utilization of a near‐cognate start codon, implicating eIF3 in AUG selection. Using in vivo cross‐linking, we observed accumulation of TC and mRNA/eIF4G on 40S subunits and a 48S ‘halfmer’ in prt1‐1 cells. Genetic evidence suggests that 40S–60S subunit joining is not rate‐limiting in the prt1‐1 mutant. Thus, eIF3b functions between 48S assembly and subunit joining to influence AUG recognition and reinitiation on GCN4 mRNA. Other mutations that disrupt eIF2–eIF3 contacts in the multifactor complex (MFC) diminished 40S‐bound TC, indicating that MFC formation enhances 43S assembly in vivo. © European Molecular Biology Organization 2004 |
collection_details |
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container_issue |
5 |
title_short |
Functions of eIF3 downstream of 48S assembly impact AUG recognition and GCN4 translational control |
url |
https://dx.doi.org/10.1038/sj.emboj.7600116 |
remote_bool |
true |
author2 |
Szamecz, Béla Valášek, Leoš Jivotovskaya, Antonina Shin, Byung‐Sik Hinnebusch, Alan G |
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Szamecz, Béla Valášek, Leoš Jivotovskaya, Antonina Shin, Byung‐Sik Hinnebusch, Alan G |
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doi_str |
10.1038/sj.emboj.7600116 |
up_date |
2024-10-20T04:49:16.488Z |
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score |
7.402135 |