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Transcription arrest relief by S‐II/TFIIS during gene expression in erythroblast differentiation
Author(s) -
Nagata Makiko,
Ito Takahiro,
Arimitsu Nagisa,
Koyama Hiroshi,
Sekimizu Kazuhisa
Publication year - 2009
Publication title -
genes to cells
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.912
H-Index - 115
eISSN - 1365-2443
pISSN - 1356-9597
DOI - 10.1111/j.1365-2443.2008.01277.x
Subject(s) - rna polymerase ii , biology , transcription (linguistics) , microbiology and biotechnology , gene expression , chromatin , histone , erythroblast , gene , promoter , genetics , haematopoiesis , linguistics , philosophy , stem cell
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 β 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 β major ‐globin gene during erythroblast differentiation, by relieving transcription arrest or affecting histone modification on chromatin template.