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Core promoter activity contributes to chromatin-based regulation of internal cryptic promoters.
Lee, Bo Bae; Woo, Hyeonju; Lee, Min Kyung; Youn, SeoJung; Lee, Sumin; Roe, Jae-Seok; Lee, Soo Young; Kim, TaeSoo.
Afiliação
  • Lee BB; Department of Life Science and the Research Center for Cellular Homeostasis, Ewha Womans University, Seoul 03760, Korea.
  • Woo H; Department of Life Science and the Research Center for Cellular Homeostasis, Ewha Womans University, Seoul 03760, Korea.
  • Lee MK; Department of Life Science and the Research Center for Cellular Homeostasis, Ewha Womans University, Seoul 03760, Korea.
  • Youn S; Department of Life Science and the Research Center for Cellular Homeostasis, Ewha Womans University, Seoul 03760, Korea.
  • Lee S; Department of Life Science and the Research Center for Cellular Homeostasis, Ewha Womans University, Seoul 03760, Korea.
  • Roe JS; Department of Biochemistry, College of Life Science and Biotechnology, Yonsei University, Seoul 03722, Korea.
  • Lee SY; Department of Life Science and the Research Center for Cellular Homeostasis, Ewha Womans University, Seoul 03760, Korea.
  • Kim T; Department of Life Science and the Research Center for Cellular Homeostasis, Ewha Womans University, Seoul 03760, Korea.
Nucleic Acids Res ; 49(14): 8097-8109, 2021 08 20.
Article em En | MEDLINE | ID: mdl-34320189
During RNA polymerase II (RNA Pol II) transcription, the chromatin structure undergoes dynamic changes, including opening and closing of the nucleosome to enhance transcription elongation and fidelity. These changes are mediated by transcription elongation factors, including Spt6, the FACT complex, and the Set2-Rpd3S HDAC pathway. These factors not only contribute to RNA Pol II elongation, reset the repressive chromatin structures after RNA Pol II has passed, thereby inhibiting aberrant transcription initiation from the internal cryptic promoters within gene bodies. Notably, the internal cryptic promoters of infrequently transcribed genes are sensitive to such chromatin-based regulation but those of hyperactive genes are not. To determine why, the weak core promoters of genes that generate cryptic transcripts in cells lacking transcription elongation factors (e.g. STE11) were replaced with those from more active genes. Interestingly, as core promoter activity increased, activation of internal cryptic promoter dropped. This associated with loss of active histone modifications at the internal cryptic promoter. Moreover, environmental changes and transcription elongation factor mutations that downregulated the core promoters of highly active genes concomitantly increased their cryptic transcription. We therefore propose that the chromatin-based regulation of internal cryptic promoters is mediated by core promoter strength as well as transcription elongation factors.
Assuntos

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: RNA Polimerase II / Cromatina / MAP Quinase Quinase Quinases / Proteínas de Saccharomyces cerevisiae / Fatores de Elongação da Transcrição / Chaperonas de Histonas / Metiltransferases Idioma: En Revista: Nucleic Acids Res Ano de publicação: 2021 Tipo de documento: Article

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: RNA Polimerase II / Cromatina / MAP Quinase Quinase Quinases / Proteínas de Saccharomyces cerevisiae / Fatores de Elongação da Transcrição / Chaperonas de Histonas / Metiltransferases Idioma: En Revista: Nucleic Acids Res Ano de publicação: 2021 Tipo de documento: Article