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<p>Human RNA polymerase II (Pol II) regulates transcription of significant number of snRNA and proliferation-related mRNA genes by involving Little Elongation Complex (LEC) and Super Elongation Complex (SEC) respectively. However, underlying mechanisms of these differential involvements of Pol II are not known. In this study, we show that human ELL, through its dynamic differential association within LEC and SEC, controls expression of target snRNA and proliferation-related mRNA genes by regulating Pol II recruitment. Mechanistically, we show that p300-mediated acetylation of Lysine 355 (K355) residue favors ELL monomerization and corresponding ELL•SEC formation and proliferation-related mRNA transcription; and reciprocally, HDAC1-mediated deacetylation favors dimerization and subsequent ELL●LEC formation and snRNA transcription; and vice versa. Physiologically, we show that whereas, mitogen treatment enhances AKT signaling-dependent p300-mediated ELL(K355) acetylation leading to increased ELL●SEC assembly and corresponding proliferation-related mRNA transcription, genotoxic stress causes ATM-mediated ELL phosphorylation-dependent deacetylation of ELL(K355) by Sin3A●HDAC1 complex causing enhanced ELL●LEC assembly and snRNA transcription.</p>

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Dynamic partitioning of a critical elongation factor between LEC and SEC regulates cellular snRNA and proliferation-related mRNA transcription

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年4月27日

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  • Arijit Nandy,
  • Sambit Dalui,
  • Prathama Talukdar,
  • Poushali Chakraborty,
  • Gaurav Bhagat,
  • Ekjot Kaur Minhas,
  • Srerupa Roy,
  • Abhishake Lahiri,
  • Venkatesha Basrur,
  • Debabrata Biswas

摘要

Human RNA polymerase II (Pol II) regulates transcription of significant number of snRNA and proliferation-related mRNA genes by involving Little Elongation Complex (LEC) and Super Elongation Complex (SEC) respectively. However, underlying mechanisms of these differential involvements of Pol II are not known. In this study, we show that human ELL, through its dynamic differential association within LEC and SEC, controls expression of target snRNA and proliferation-related mRNA genes by regulating Pol II recruitment. Mechanistically, we show that p300-mediated acetylation of Lysine 355 (K355) residue favors ELL monomerization and corresponding ELL•SEC formation and proliferation-related mRNA transcription; and reciprocally, HDAC1-mediated deacetylation favors dimerization and subsequent ELL●LEC formation and snRNA transcription; and vice versa. Physiologically, we show that whereas, mitogen treatment enhances AKT signaling-dependent p300-mediated ELL(K355) acetylation leading to increased ELL●SEC assembly and corresponding proliferation-related mRNA transcription, genotoxic stress causes ATM-mediated ELL phosphorylation-dependent deacetylation of ELL(K355) by Sin3A●HDAC1 complex causing enhanced ELL●LEC assembly and snRNA transcription.