p53 represses the transcription of snRNA genes by preventing the formation of little elongation complex.
The regulation of transcription by RNA polymerase II (Pol II) is important for a variety of cellular functions. ELL/EAF-containing little elongation complex (LEC) was found to be required for transcription of Pol II-dependent small nuclear RNA (snRNA) genes. It was shown that the tumor suppressor p53 interacts with ELL and inhibits transcription elongation activity of ELL. Here, we show that p53 inhibits interaction between ELL/EAF and ICE1 in LEC and thereby p53 represses transcription of Pol II-dependent snRNA genes through inhibiting LEC function. Furthermore, induction of p53 expression by ultraviolet (UV) irradiation decreases the occupancy of ICE1 at Pol II-dependent snRNA genes. Consistent with the results, knockdown of p53 increased both the expression of snRNA genes and the occupancy of Pol II and components of LEC at snRNA genes. Our results indicate that p53 interferes with the interaction between ELL/EAF and ICE1 and represses transcription of snRNA genes by Pol II.
Department of Biochemistry, Hokkaido University Graduate School of Medicine, Sapporo, Hokkaido 060-8638, Japan; Department of Otolaryngology, Head & Neck Surgery, Hokkaido University Graduate School of Medicine, Sapporo, Hokkaido 060-8638, Japan.
Delnur
D
Anwar
Department of Biochemistry, Hokkaido University Graduate School of Medicine, Sapporo, Hokkaido 060-8638, Japan.
Hidehisa
H
Takahashi
Department of Biochemistry, Hokkaido University Graduate School of Medicine, Sapporo, Hokkaido 060-8638, Japan.
Masashi
M
Watanabe
Department of Biochemistry, Hokkaido University Graduate School of Medicine, Sapporo, Hokkaido 060-8638, Japan; Department of Otolaryngology, Head & Neck Surgery, Hokkaido University Graduate School of Medicine, Sapporo, Hokkaido 060-8638, Japan.
Masanobu
M
Suzuki
Department of Otolaryngology, Head & Neck Surgery, Hokkaido University Graduate School of Medicine, Sapporo, Hokkaido 060-8638, Japan.
Satoshi
S
Fukuda
Department of Biochemistry, Hokkaido University Graduate School of Medicine, Sapporo, Hokkaido 060-8638, Japan. Electronic address: hatas@med.hokudai.ac.jp.
Shigetsugu
S
Hatakeyama
D000818:Animals; D016367:Baculoviridae / Q000235:genetics / Q000378:metabolism; D002352:Carrier Proteins / Q000235:genetics* / Q000378:metabolism; D003001:Cloning, Molecular; D005786:Gene Expression Regulation; D045325:HCT116 Cells; D006801:Humans; D012319:RNA Polymerase II / Q000235:genetics* / Q000378:metabolism; D012342:RNA, Small Nuclear / Q000235:genetics* / Q000378:metabolism; D011994:Recombinant Proteins / Q000235:genetics / Q000378:metabolism; D061987:Sf9 Cells; D015398:Signal Transduction; D018411:Spodoptera; D014158:Transcription, Genetic; D035602:Transcriptional Elongation Factors / Q000235:genetics* / Q000378:metabolism; D016159:Tumor Suppressor Protein p53 / Q000235:genetics* / Q000378:metabolism; D014466:Ultraviolet Rays
D002352:Carrier Proteins; C090862:ELL protein, human; C000620192:ICE1 protein, human; D012342:RNA, Small Nuclear; D011994:Recombinant Proteins; D035602:Transcriptional Elongation Factors; D016159:Tumor Suppressor Protein p53; D012319:RNA Polymerase II
ELL; LEC; Transcription; p53; snRNA