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Genome-wide interference of chromatin architecture and Mediator in transcriptional bursting and gene network regulation

ABSTRACT: Gene expression is a stochastic process that occurs in bursts of RNA synthesis. We applied a mathematical model to scRNA-Seq data to infer bursting dynamics transcriptome-wide under multiple perturbations in a wide range of cell types and identified possible molecular mechanisms. We find that mediator complex subunit MED26 primarily regulates frequency, MYC regulates burst size, while cohesin and super-enhancers can modulate both. Despite comparable effect sizes on RNA levels amongst these perturbations, we find that acute depletion of MED26 plays a larger role in perturbing gene regulatory networks. Furthermore, this perturbation acts downstream of both chromatin spatial architecture and preinitiation complex formation, indicating that later steps in the initiation of transcriptional bursts are primary nodes for integrating gene networks in single cells.

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE241338 | GEO | 2024/06/30

REPOSITORIES: GEO

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Project description:This a model from the article: Complex bursting in pancreatic islets: a potential glycolytic mechanism. Wierschem K, Bertram R. J Theor Biol 2004 Jun 21;228(4):513-21 15178199 , Abstract: The electrical activity of insulin-secreting pancreatic islets of Langerhans is characterized by bursts of action potentials. Most often this bursting is periodic, but in some cases it is modulated by an underlying slower rhythm. We suggest that the modulatory rhythm for this complex bursting pattern is due to oscillations in glycolysis, while the bursting itself is generated by some other slow process. To demonstrate this hypothesis, we couple a minimal model of glycolytic oscillations to a minimal model for activity-dependent bursting in islets. We show that the combined model can reproduce several complex bursting patterns from mouse islets published in the literature, and we illustrate how these complex oscillations are produced through the use of a fast/slow analysis. This model was taken from the CellML repository and automatically converted to SBML. The original model was: Wierschem K, Bertram R. () - version=1.0 The original CellML model was created by: Ethan Choi mcho099@aucklanduni.ac.nz The University of Auckland This model originates from BioModels Database: A Database of Annotated Published Models (http://www.ebi.ac.uk/biomodels/). It is copyright (c) 2005-2011 The BioModels.net Team. To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication for more information. In summary, you are entitled to use this encoded model in absolutely any manner you deem suitable, verbatim, or with modification, alone or embedded it in a larger context, redistribute it, commercially or not, in a restricted way or not.. To cite BioModels Database, please use: Li C, Donizelli M, Rodriguez N, Dharuri H, Endler L, Chelliah V, Li L, He E, Henry A, Stefan MI, Snoep JL, Hucka M, Le Novère N, Laibe C (2010) BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. BMC Syst Biol., 4:92.

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Genome-wide interference of chromatin architecture and Mediator in transcriptional bursting and gene network regulation

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