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PreprintCC BY-NC 4.0Genes and Development

Mitotic MAX bookmarking drives MYC-dependent hypertranscription at TBP-bound promoters

  • Inma Gonzalez1,2
  • Lieng Taing1,2
  • Almira Chervova1,2
  • Pedro Escoll3
  • Luis Altamirano-Pacheco1,4
  • Alina Sommer4,5
  • Teresa Urli6
  • Maxim V.C. Greenberg6
  • Véronique Legros6
  • Guillaume Chevreux6
  • Florian Mueller7
  • Agnès Dubois1,2
1 more authors
  • Pablo Navarro1,2
7 affiliations
  1. 1Department of Developmental and Stem Cell Biology, Institut Pasteur, Université Paris Cité, CNRS UMR3738, Epigenomics, Proliferation, and the Identity of Cells Unit, Paris 75015, France
  2. 2Equipe Labélisée Ligue Contre le Cancer, Paris 75015, France
  3. 3Department of Microbiology, Institut Pasteur, Université Paris Cité, CNRS UMR 6047, Biologie des Bactéries Intracellulaires, Paris 75015, France
  4. 4College Doctoral, Sorbonne Université, Paris 75006, France
  5. 5Department of Developmental and Stem Cell Biology, Institut Pasteur, Université Paris Cité, CNRS UMR3738, Macrophages and Endothelial Cells Unit, Paris 75015, France
  6. 6Université Paris Cité, CNRS, Institut Jacques Monod, Paris 75013, France
  7. 7Centre de Ressources et Recherches Technologiques (UTechS-PBI, C2RT), Institut Pasteur, Université Paris Cité, CNRS UMR3691, Photonic Bio-Imaging, Paris 75015, France
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Abstract

Faithful genome reactivation after mitosis is essential for cell identity, yet the mechanisms driving global postmitotic transcription remain unclear. Here, we show that the MYC oncogene and its obligate partner MAX drive a postmitotic hypertranscriptional state in mouse embryonic stem cells. Cell cycle–resolved single-cell RNA-seq in inducible Max −/− cells reveals that early G1 hypertranscription is strongly impaired without MAX. Mechanistically, MAX remains bound to thousands of promoters during mitosis, while MYC is largely excluded. Using high-temporal-resolution profiling, pharmacological inhibition of MYC/MAX, and acute MAX degradation at mitotic exit, we demonstrate that MAX mitotic binding triggers rapid MYC recruitment and transcriptional amplification of TBP-bound promoters by enhancing RNA polymerase II occupancy and efficient initiation and elongation. These findings redefine MYC/MAX as master regulators of gene regulatory inheritance across mitosis.

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Cite

BibTeXRIS
BibTeX
@misc{gonzalez2026mitotic,
  title = {{Mitotic MAX bookmarking drives MYC-dependent hypertranscription at TBP-bound promoters}},
  author = {Inma Gonzalez and Lieng Taing and Almira Chervova and Pedro Escoll and Luis Altamirano-Pacheco and Alina Sommer and Teresa Urli and Maxim V.C. Greenberg and Véronique Legros and Guillaume Chevreux and Florian Mueller and Agnès Dubois and Pablo Navarro},
  howpublished = {Genes and Development},
  year = {2026},
  month = aug,
  doi = {10.1101/gad.354072.126},
  url = {https://hal.science/hal-05768909v1},
  note = {CC BY-NC 4.0},
}
RIS
TY  - UNPB
TI  - Mitotic MAX bookmarking drives MYC-dependent hypertranscription at TBP-bound promoters
AU  - Inma Gonzalez
AU  - Lieng Taing
AU  - Almira Chervova
AU  - Pedro Escoll
AU  - Luis Altamirano-Pacheco
AU  - Alina Sommer
AU  - Teresa Urli
AU  - Maxim V.C. Greenberg
AU  - Véronique Legros
AU  - Guillaume Chevreux
AU  - Florian Mueller
AU  - Agnès Dubois
AU  - Pablo Navarro
PY  - 2026
DA  - 2026/08/06
PB  - Genes and Development
DO  - 10.1101/gad.354072.126
UR  - https://hal.science/hal-05768909v1
AB  - Faithful genome reactivation after mitosis is essential for cell identity, yet the mechanisms driving global postmitotic transcription remain unclear. Here, we show that the MYC oncogene and its obligate partner MAX drive a postmitotic hypertranscriptional state in mouse embryonic stem cells. Cell cycle–resolved single-cell RNA-seq in inducible Max −/− cells reveals that early G1 hypertranscription is strongly impaired without MAX. Mechanistically, MAX remains bound to thousands of promoters during mitosis, while MYC is largely excluded. Using high-temporal-resolution profiling, pharmacological inhibition of MYC/MAX, and acute MAX degradation at mitotic exit, we demonstrate that MAX mitotic binding triggers rapid MYC recruitment and transcriptional amplification of TBP-bound promoters by enhancing RNA polymerase II occupancy and efficient initiation and elongation. These findings redefine MYC/MAX as master regulators of gene regulatory inheritance across mitosis.
SN  - 0890-9369
SN  - 1549-5477
ER  -