Evidence map›Paper›PMID 42045218›Full record

ArticleNature communications2026

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

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

Abstract read
In one paragraph

Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors.

Arijit NandyLaboratory of Transcription Biology, Cell Biology and Physiology Division, CSIR-Indian Institute of Chemical Biology, Kolkata, India.
Sambit DaluiDivision of Hematology, The Children's Hospital of Philadelphia, Philadelphia, PA, USA.
Prathama Talukdar *Laboratory of Transcription Biology, Cell Biology and Physiology Division, CSIR-Indian Institute of Chemical Biology, Kolkata, India.
Poushali Chakraborty *Laboratory of Transcription Biology, Cell Biology and Physiology Division, CSIR-Indian Institute of Chemical Biology, Kolkata, India.
Gaurav BhagatLaboratory of Transcription Biology, Cell Biology and Physiology Division, CSIR-Indian Institute of Chemical Biology, Kolkata, India.ORCID http://orcid.org/0000-0002-9892-9437
Ekjot Kaur MinhasLaboratory of Transcription Biology, Cell Biology and Physiology Division, CSIR-Indian Institute of Chemical Biology, Kolkata, India.ORCID http://orcid.org/0009-0000-7070-2372
Srerupa RoyLaboratory of Transcription Biology, Cell Biology and Physiology Division, CSIR-Indian Institute of Chemical Biology, Kolkata, India.
Abhishake LahiriAcademy of Scientific and Innovative Research (AcSIR), Ghaziabad, India.
Venkatesha BasrurDepartment of Pathology, University of Michigan, Ann Arbor, MI, USA.
Debabrata BiswasLaboratory of Transcription Biology, Cell Biology and Physiology Division, CSIR-Indian Institute of Chemical Biology, Kolkata, India. dbiswas@iicb.res.in.ORCID http://orcid.org/0000-0002-6782-6398

Funding

DBT India Alliance (Wellcome Trust/DBT India Alliance) IA/S/22/1/506227DST | Science and Engineering Research Board (SERB) CRG/2022/000756
6 · The paper itself

Abstract

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.

Indexed as

RNA, MessengerRNA, Small NuclearTranscriptional Elongation FactorsTranscription, GeneticAcetylationCell ProliferationE1A-Associated p300 ProteinHistone Deacetylase 1HumansPhosphorylationRNA Polymerase IIE1A-Associated p300 ProteinEP300 protein, humanHDAC1 protein, humanHistone Deacetylase 1RNA, MessengerRNA Polymerase IIRNA, Small NuclearTranscriptional Elongation Factors

Identifiers

PMID42045218
PMCPMC13324577

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.