| First Author | Nagata M | Year | 2009 |
| Journal | Genes Cells | Volume | 14 |
| Issue | 3 | Pages | 371-80 |
| PubMed ID | 19210546 | Mgi Jnum | J:146843 |
| Mgi Id | MGI:3838671 | Doi | 10.1111/j.1365-2443.2008.01277.x |
| Citation | Nagata M, et al. (2009) Transcription arrest relief by S-II/TFIIS during gene expression in erythroblast differentiation. Genes Cells 14(3):371-80 |
| abstractText | Transcription stimulator S-II relieves RNA polymerase II (RNAPII) from transcription elongation arrest. Mice lacking the S-II gene (S-II KO mice) die at mid-gestation with impaired erythroblast differentiation, and have decreased expression of the Bcl-x gene. To understand a role of S-II in Bcl-x gene expression, we examined the distribution of transcription complex on the Bcl-x gene in S-II KO mice. The amount of RNAPII at intron 2 of the Bcl-x gene was decreased in S-II KO mice, whereas recruitment of transcription initiation factor TFIIB and RNAPII to the promoter was not decreased. Consistently, in vitro transcription analysis revealed the presence of a transcription arrest site in the Bcl-x gene intron 2, and transcription arrest at this site was overcome by S-II. Furthermore, histone acetylation on the coding region of the Bcl-x gene was decreased in S-II KO mice. In the beta(major)-globin gene, whose expression was also decreased in S-II KO mice, there were no changes in RNAPII distribution or histone acetylation, but the amount of histone H3 occupying the coding region was increased. These results suggest that S-II is involved in transcription of the Bcl-x and beta(major)-globin gene during erythroblast differentiation, by relieving transcription arrest or affecting histone modification on chromatin template. |
