STAT3 and Oct-3/4 Control Histone Modification through Induction of Eed in Embryonic Stem Cells
Mouse embryonic stem (ES) cells can self-renew in the presence of leukemia inhibitory factor (LIF). Several essential transcription factors have been identified for the self-renewal of mouse ES cells, including STAT3, Oct-3/4, and Nanog. The molecular mechanism of ES cell self-renewal, however, is n...
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| Veröffentlicht in: | The Journal of biological chemistry 2008-04, Vol.283 (15), p.9713-9723 |
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| container_title | The Journal of biological chemistry |
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| creator | Ura, Hiroki Usuda, Masayuki Kinoshita, Keita Sun, Chuanhai Mori, Keitaro Akagi, Tadayuki Matsuda, Takahiko Koide, Hiroshi Yokota, Takashi |
| description | Mouse embryonic stem (ES) cells can self-renew in the presence of leukemia inhibitory factor (LIF). Several essential transcription factors have been identified for the self-renewal of mouse ES cells, including STAT3, Oct-3/4, and Nanog. The molecular mechanism of ES cell self-renewal, however, is not fully understood. In the present study, we identified Eed, a core component of Polycomb repressive complex 2, as a downstream molecule of STAT3 and Oct-3/4. Artificial activation of STAT3 resulted in increased expression of Eed, whereas expression of a dominant negative mutant of STAT3 or suppression of Oct-3/4 expression led to down-regulation of Eed. Reporter, chromatin immunoprecipitation, and electrophoretic mobility shift assays revealed that STAT3 and Oct-3/4 directly bind to the promoter region of Eed, suggesting that Eed is a common target molecule of STAT3 and Oct-3/4. We also found that suppression of STAT3, Oct-3/4, or Eed causes induction of differentiation-associated genes as well as loss of Lys27-trimethylated histone H3 at the promoter regions of the differentiation-associated genes. Suppression of STAT3 and Oct-3/4 also resulted in the absence of Eed at the promoter regions. These results suggest that STAT3 and Oct-3/4 maintain silencing of differentiation-associated genes through up-regulation of Eed in self-renewing ES cells. |
| doi_str_mv | 10.1074/jbc.M707275200 |
| format | Article |
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Several essential transcription factors have been identified for the self-renewal of mouse ES cells, including STAT3, Oct-3/4, and Nanog. The molecular mechanism of ES cell self-renewal, however, is not fully understood. In the present study, we identified Eed, a core component of Polycomb repressive complex 2, as a downstream molecule of STAT3 and Oct-3/4. Artificial activation of STAT3 resulted in increased expression of Eed, whereas expression of a dominant negative mutant of STAT3 or suppression of Oct-3/4 expression led to down-regulation of Eed. Reporter, chromatin immunoprecipitation, and electrophoretic mobility shift assays revealed that STAT3 and Oct-3/4 directly bind to the promoter region of Eed, suggesting that Eed is a common target molecule of STAT3 and Oct-3/4. We also found that suppression of STAT3, Oct-3/4, or Eed causes induction of differentiation-associated genes as well as loss of Lys27-trimethylated histone H3 at the promoter regions of the differentiation-associated genes. Suppression of STAT3 and Oct-3/4 also resulted in the absence of Eed at the promoter regions. These results suggest that STAT3 and Oct-3/4 maintain silencing of differentiation-associated genes through up-regulation of Eed in self-renewing ES cells.</description><identifier>ISSN: 0021-9258</identifier><identifier>EISSN: 1083-351X</identifier><identifier>DOI: 10.1074/jbc.M707275200</identifier><identifier>PMID: 18201968</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Animals ; Cell Differentiation - physiology ; Cell Line ; Cell Proliferation ; DNA-Binding Proteins - genetics ; DNA-Binding Proteins - metabolism ; Embryonic Stem Cells - cytology ; Embryonic Stem Cells - metabolism ; Gene Silencing - physiology ; Homeodomain Proteins - genetics ; Homeodomain Proteins - metabolism ; Humans ; Leukemia Inhibitory Factor - pharmacology ; Mice ; Nanog Homeobox Protein ; Octamer Transcription Factor-3 - genetics ; Octamer Transcription Factor-3 - metabolism ; Polycomb Repressive Complex 2 ; Promoter Regions, Genetic - physiology ; Protein Binding - physiology ; Repressor Proteins - biosynthesis ; Repressor Proteins - genetics ; STAT3 Transcription Factor - genetics ; STAT3 Transcription Factor - metabolism</subject><ispartof>The Journal of biological chemistry, 2008-04, Vol.283 (15), p.9713-9723</ispartof><rights>2008 © 2008 ASBMB. 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Several essential transcription factors have been identified for the self-renewal of mouse ES cells, including STAT3, Oct-3/4, and Nanog. The molecular mechanism of ES cell self-renewal, however, is not fully understood. In the present study, we identified Eed, a core component of Polycomb repressive complex 2, as a downstream molecule of STAT3 and Oct-3/4. Artificial activation of STAT3 resulted in increased expression of Eed, whereas expression of a dominant negative mutant of STAT3 or suppression of Oct-3/4 expression led to down-regulation of Eed. Reporter, chromatin immunoprecipitation, and electrophoretic mobility shift assays revealed that STAT3 and Oct-3/4 directly bind to the promoter region of Eed, suggesting that Eed is a common target molecule of STAT3 and Oct-3/4. We also found that suppression of STAT3, Oct-3/4, or Eed causes induction of differentiation-associated genes as well as loss of Lys27-trimethylated histone H3 at the promoter regions of the differentiation-associated genes. Suppression of STAT3 and Oct-3/4 also resulted in the absence of Eed at the promoter regions. 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We also found that suppression of STAT3, Oct-3/4, or Eed causes induction of differentiation-associated genes as well as loss of Lys27-trimethylated histone H3 at the promoter regions of the differentiation-associated genes. Suppression of STAT3 and Oct-3/4 also resulted in the absence of Eed at the promoter regions. These results suggest that STAT3 and Oct-3/4 maintain silencing of differentiation-associated genes through up-regulation of Eed in self-renewing ES cells.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>18201968</pmid><doi>10.1074/jbc.M707275200</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Cell Differentiation - physiology Cell Line Cell Proliferation DNA-Binding Proteins - genetics DNA-Binding Proteins - metabolism Embryonic Stem Cells - cytology Embryonic Stem Cells - metabolism Gene Silencing - physiology Homeodomain Proteins - genetics Homeodomain Proteins - metabolism Humans Leukemia Inhibitory Factor - pharmacology Mice Nanog Homeobox Protein Octamer Transcription Factor-3 - genetics Octamer Transcription Factor-3 - metabolism Polycomb Repressive Complex 2 Promoter Regions, Genetic - physiology Protein Binding - physiology Repressor Proteins - biosynthesis Repressor Proteins - genetics STAT3 Transcription Factor - genetics STAT3 Transcription Factor - metabolism |
| title | STAT3 and Oct-3/4 Control Histone Modification through Induction of Eed in Embryonic Stem Cells |
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