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mTOR-dependent activation of the transcription factor TIF-IA links rRNA synthesis to nutrient availability
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| Zeitschriftentitel: | Genes & Development |
|---|---|
| Personen und Körperschaften: | , , , |
| In: | Genes & Development, 18, 2004, 4, S. 423-434 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
Cold Spring Harbor Laboratory
|
| Schlagwörter: |
| author_facet |
Mayer, Christine Zhao, Jian Yuan, Xuejun Grummt, Ingrid Mayer, Christine Zhao, Jian Yuan, Xuejun Grummt, Ingrid |
|---|---|
| author |
Mayer, Christine Zhao, Jian Yuan, Xuejun Grummt, Ingrid |
| spellingShingle |
Mayer, Christine Zhao, Jian Yuan, Xuejun Grummt, Ingrid Genes & Development mTOR-dependent activation of the transcription factor TIF-IA links rRNA synthesis to nutrient availability Developmental Biology Genetics |
| author_sort |
mayer, christine |
| spelling |
Mayer, Christine Zhao, Jian Yuan, Xuejun Grummt, Ingrid 0890-9369 1549-5477 Cold Spring Harbor Laboratory Developmental Biology Genetics http://dx.doi.org/10.1101/gad.285504 <jats:p>In cycling cells, transcription of ribosomal RNA genes by RNA polymerase I (Pol I) is tightly coordinated with cell growth. Here, we show that the mammalian target of rapamycin (mTOR) regulates Pol I transcription by modulating the activity of TIF-IA, a regulatory factor that senses nutrient and growth-factor availability. Inhibition of mTOR signaling by rapamycin inactivates TIF-IA and impairs transcription-initiation complex formation. Moreover, rapamycin treatment leads to translocation of TIF-IA into the cytoplasm. Rapamycin-mediated inactivation of TIF-IA is caused by hypophosphorylation of Ser 44 (S44) and hyperphosphorylation of Ser 199 (S199). Phosphorylation at these sites affects TIF-IA activity in opposite ways, for example, phosphorylation of S44 activates and S199 inactivates TIF-IA. The results identify a new target for mTOR-signaling pathways and elucidate the molecular mechanism underlying mTOR-dependent regulation of rRNA synthesis.</jats:p> mTOR-dependent activation of the transcription factor TIF-IA links rRNA synthesis to nutrient availability Genes & Development |
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| title |
mTOR-dependent activation of the transcription factor TIF-IA links rRNA synthesis to nutrient availability |
| title_unstemmed |
mTOR-dependent activation of the transcription factor TIF-IA links rRNA synthesis to nutrient availability |
| title_full |
mTOR-dependent activation of the transcription factor TIF-IA links rRNA synthesis to nutrient availability |
| title_fullStr |
mTOR-dependent activation of the transcription factor TIF-IA links rRNA synthesis to nutrient availability |
| title_full_unstemmed |
mTOR-dependent activation of the transcription factor TIF-IA links rRNA synthesis to nutrient availability |
| title_short |
mTOR-dependent activation of the transcription factor TIF-IA links rRNA synthesis to nutrient availability |
| title_sort |
mtor-dependent activation of the transcription factor tif-ia links rrna synthesis to nutrient availability |
| topic |
Developmental Biology Genetics |
| url |
http://dx.doi.org/10.1101/gad.285504 |
| publishDate |
2004 |
| physical |
423-434 |
| description |
<jats:p>In cycling cells, transcription of ribosomal RNA genes by RNA polymerase I (Pol I) is tightly coordinated with cell growth. Here, we show that the mammalian target of rapamycin (mTOR) regulates Pol I transcription by modulating the activity of TIF-IA, a regulatory factor that senses nutrient and growth-factor availability. Inhibition of mTOR signaling by rapamycin inactivates TIF-IA and impairs transcription-initiation complex formation. Moreover, rapamycin treatment leads to translocation of TIF-IA into the cytoplasm. Rapamycin-mediated inactivation of TIF-IA is caused by hypophosphorylation of Ser 44 (S44) and hyperphosphorylation of Ser 199 (S199). Phosphorylation at these sites affects TIF-IA activity in opposite ways, for example, phosphorylation of S44 activates and S199 inactivates TIF-IA. The results identify a new target for mTOR-signaling pathways and elucidate the molecular mechanism underlying mTOR-dependent regulation of rRNA synthesis.</jats:p> |
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| author | Mayer, Christine, Zhao, Jian, Yuan, Xuejun, Grummt, Ingrid |
| author_facet | Mayer, Christine, Zhao, Jian, Yuan, Xuejun, Grummt, Ingrid, Mayer, Christine, Zhao, Jian, Yuan, Xuejun, Grummt, Ingrid |
| author_sort | mayer, christine |
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| description | <jats:p>In cycling cells, transcription of ribosomal RNA genes by RNA polymerase I (Pol I) is tightly coordinated with cell growth. Here, we show that the mammalian target of rapamycin (mTOR) regulates Pol I transcription by modulating the activity of TIF-IA, a regulatory factor that senses nutrient and growth-factor availability. Inhibition of mTOR signaling by rapamycin inactivates TIF-IA and impairs transcription-initiation complex formation. Moreover, rapamycin treatment leads to translocation of TIF-IA into the cytoplasm. Rapamycin-mediated inactivation of TIF-IA is caused by hypophosphorylation of Ser 44 (S44) and hyperphosphorylation of Ser 199 (S199). Phosphorylation at these sites affects TIF-IA activity in opposite ways, for example, phosphorylation of S44 activates and S199 inactivates TIF-IA. The results identify a new target for mTOR-signaling pathways and elucidate the molecular mechanism underlying mTOR-dependent regulation of rRNA synthesis.</jats:p> |
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| imprint_str_mv | Cold Spring Harbor Laboratory, 2004 |
| institution | DE-Bn3, DE-Brt1, DE-Zwi2, DE-D161, DE-Gla1, DE-Zi4, DE-15, DE-Pl11, DE-Rs1, DE-105, DE-14, DE-Ch1, DE-L229, DE-D275 |
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| physical | 423-434 |
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| series | Genes & Development |
| source_id | 49 |
| spelling | Mayer, Christine Zhao, Jian Yuan, Xuejun Grummt, Ingrid 0890-9369 1549-5477 Cold Spring Harbor Laboratory Developmental Biology Genetics http://dx.doi.org/10.1101/gad.285504 <jats:p>In cycling cells, transcription of ribosomal RNA genes by RNA polymerase I (Pol I) is tightly coordinated with cell growth. Here, we show that the mammalian target of rapamycin (mTOR) regulates Pol I transcription by modulating the activity of TIF-IA, a regulatory factor that senses nutrient and growth-factor availability. Inhibition of mTOR signaling by rapamycin inactivates TIF-IA and impairs transcription-initiation complex formation. Moreover, rapamycin treatment leads to translocation of TIF-IA into the cytoplasm. Rapamycin-mediated inactivation of TIF-IA is caused by hypophosphorylation of Ser 44 (S44) and hyperphosphorylation of Ser 199 (S199). Phosphorylation at these sites affects TIF-IA activity in opposite ways, for example, phosphorylation of S44 activates and S199 inactivates TIF-IA. The results identify a new target for mTOR-signaling pathways and elucidate the molecular mechanism underlying mTOR-dependent regulation of rRNA synthesis.</jats:p> mTOR-dependent activation of the transcription factor TIF-IA links rRNA synthesis to nutrient availability Genes & Development |
| spellingShingle | Mayer, Christine, Zhao, Jian, Yuan, Xuejun, Grummt, Ingrid, Genes & Development, mTOR-dependent activation of the transcription factor TIF-IA links rRNA synthesis to nutrient availability, Developmental Biology, Genetics |
| title | mTOR-dependent activation of the transcription factor TIF-IA links rRNA synthesis to nutrient availability |
| title_full | mTOR-dependent activation of the transcription factor TIF-IA links rRNA synthesis to nutrient availability |
| title_fullStr | mTOR-dependent activation of the transcription factor TIF-IA links rRNA synthesis to nutrient availability |
| title_full_unstemmed | mTOR-dependent activation of the transcription factor TIF-IA links rRNA synthesis to nutrient availability |
| title_short | mTOR-dependent activation of the transcription factor TIF-IA links rRNA synthesis to nutrient availability |
| title_sort | mtor-dependent activation of the transcription factor tif-ia links rrna synthesis to nutrient availability |
| title_unstemmed | mTOR-dependent activation of the transcription factor TIF-IA links rRNA synthesis to nutrient availability |
| topic | Developmental Biology, Genetics |
| url | http://dx.doi.org/10.1101/gad.285504 |