Canonical and atypical E2Fs regulate the mammalian endocycle
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The endocycle is a variant cell cycle consisting of successive DNA synthesis and gap phases that yield highly polyploid cells. Although essential for metazoan development, relatively little is known about its control or physiologic role in mammals. Using lineage-specific cre mice we identified two opposing arms of the E2F program, one driven by canonical transcription activation (E2F1, E2F2 and E2F3) and the other by atypical repression (E2F7 and E2F8), that converge on the regulation of endocycles in vivo. Ablation of canonical activators in the two endocycling tissues of mammals, trophoblast giant cells in the placenta and hepatocytes in the liver, augmented genome ploidy, whereas ablation of atypical repressors diminished ploidy. These two antagonistic arms coordinate the expression of a unique G2/M transcriptional program that is critical for mitosis, karyokinesis and cytokinesis. These results provide in vivo evidence for a direct role of E2F family members in regulating non-traditional cell cycles in mammals.
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E2F7 and E2F8 inhibit expression of many genes including Aurka/b, Ccnb1, and Plk1.
“Acting as mutually redundant transcriptional repressors, E2F7 and E2F8 inhibit the expression of many genes, including Aurka/b, Ccnb1, and Plk1, which encode proteins that act during mitotic progression (7, 8, 11).”
From Wnt signaling regulates hepatocyte cell division by a transcriptional repressor cascade (2022) · cites this paper as [7]
The Results section, “E2F7/E2F8 Regulate Endocycle-related Genes” (page unavailable), reports that loss of E2F7 or E2F8 derepresses many genes, including genes involved in G2/M progression and mitosis. Our copy does not identify Aurka, Aurkb, Ccnb1, or Plk1 as genes whose expression they inhibit, so it supports the general point but not the named examples. (LLM, conf=0.84)
Experimental — accuracy not yet measuredE2F7 and E2F8 are responsible for cell cycle arrest in the liver.
“Two members of the E2F family of cell cycle regulators, E2F7 and E2F8, are responsible for this form of cell cycle arrest in the liver (Chen et al. 2012;Pandit et al. 2012).”
From Hepatocyte Cell Cycle Progression Depends on a Transcriptional Repressor Cascade Downstream of Wnt Signaling (2021) · cites this paper as Chen et al. 2012
The Results sections on hepatocyte endocycles and endocycle-related genes show that E2F7 and E2F8 help suppress mitosis in mouse hepatocytes, with E2F8 identified as the principal regulator. The paper describes a mitotic block that permits continued DNA replication, not a general arrest of the cell cycle; the claim omits that distinction. (LLM, conf=0.82)
Experimental — accuracy not yet measuredIn the liver, E2f7 and E2f8 are responsible for cell cycle arrest that uncouples DNA synthesis from proliferation.
“In the liver, two members of the E2F family of cell cycle regulators, E2f7 and E2f8, are responsible for this form of cell cycle arrest (7, 8).”
From Wnt signaling regulates hepatocyte cell division by a transcriptional repressor cascade (2022) · cites this paper as [7]
Deleting E2f7 and E2f8 from hepatocytes results in completion of M phase and generation of diploid daughter cells.
“Deleting E2f7 and E2f8 from hepatocytes results in completion of M phase and the generation of diploid daughter cells (7, 8).”
From Wnt signaling regulates hepatocyte cell division by a transcriptional repressor cascade (2022) · cites this paper as [7]
In several tissues including the liver, transcriptional repressors E2F7 and E2F8 function as inhibitors of mitosis and promote polyploidy.
“In several tissues including the liver, transcriptional repressors such as E2F7 and E2F8 function as inhibitors of mitosis and promote polyploidy”
From Hepatocyte Cell Cycle Progression Depends on a Transcriptional Repressor Cascade Downstream of Wnt Signaling (2021) · cites this paper as Chen et al. 2012
In the liver, DNA synthesis is uncoupled from cell proliferation due to the activity of E2F7 and E2F8.
“Therefore, in the liver, DNA synthesis is uncoupled from cell proliferation due to the activity of E2F7 and E2F8.”
From Hepatocyte Cell Cycle Progression Depends on a Transcriptional Repressor Cascade Downstream of Wnt Signaling (2021) · cites this paper as Chen et al. 2012
Deleting E2f7 and E2f8 from liver cells results in completion of M phase and generation of diploid daughter cells.
“Deleting E2f7 and E2f8 from these cells results in completion of M phase and the generation of diploid daughter cells (Chen et al. 2012;Pandit et al. 2012).”
From Hepatocyte Cell Cycle Progression Depends on a Transcriptional Repressor Cascade Downstream of Wnt Signaling (2021) · cites this paper as Chen et al. 2012
Considering the mixture of nonparenchymal cells (30-40% of total cells) and the polyploidy of hepatocytes in the mouse liver, the deep sequencing data may be consistent with Fah+ hepatocytes.
“Nevertheless, considering the mixture of nonparenchymal cells (30–40% of total cells) and the polyploidy of hepatocytes in the mouse liver35, the deep sequencing data may be consistent with Fah+ hepatocytes.”
From Therapeutic genome editing by combined viral and non-viral delivery of CRISPR system components in vivo (2016) · cites this paper as [35]
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- Authors
- Chen, H.-Z., Ouseph, M. M., Li, J., Pécot, T., Chokshi, V., Kent, L., Bae, S., Byrne, M., Duran, C., Comstock, G., Trikha, P., Mair, M., Senapati, S., Martin, C. K., Gandhi, S., Wilson, N., Liu, B., Huang, Y.-W., Thompson, J. C., Raman, S., Singh, S., Leone, M., Machiraju, R., Huang, K., Mo, X., Fernandez, S., Kalaszczynska, I., Wolgemuth, D. J., Sicinski, P., Huang, T., Jin, V., & Leone, G.
- Affiliations
- The Ohio State University (US)
- Medical College of Wisconsin (US)
- Columbia University Irving Medical Center (US)
- Corresponding author
- Leone, Gustavo
- ORCID
- Venue
- Nature Cell Biology
- Published
- 2012-10-14
- Volume
- 14
- Issue
- 11
- Pages
- 1192-1202
- ISSN
- 1465-7392 (ISSN-L)
- 1476-4679
- PMC
- PMC3616487
- OpenAlex
- W2068278990
- Cited by
- 161
- References
- 60
- Citations by year
- 2026: 6 · 2025: 10 · 2024: 12 · 2023: 14 · 2022: 11 · 2021: 11 · 2020: 14 · 2019: 10 · 2018: 13 · 2017: 11 · 2016: 10 · 2015: 12 · 2014: 10 · 2013: 13 · 2012: 3
- FWCI
- 6.01
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Cell Biology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Digital Access to Scholarship at Harvard (DASH) (Harvard University) (submittedVersion, cc-by)
- HAL (submittedVersion)
- Minerva Access (University of Melbourne) (submittedVersion)
- Funders
- National Cancer Institute (R01 CA85619, R01 CA 82259, R01CA132740, R01CA085619, R01CA082259, P01CA097189, P30CA016058)
- National Center for Research Resources (UL1RR025755)
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (R01HD047470)
- Topics
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Developmental Biology and Gene Regulation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Microtubule and mitosis dynamics
- Keywords
- endocycle, E2F transcription factors, E2F7, E2F8, E2F1, E2F2, E2F3, polyploidy, trophoblast giant cells, hepatocytes, cell cycle regulation, transcriptional repression
- MeSH terms
- Animals, Cell Cycle, Female, Flow Cytometry, Immunohistochemistry, Microscopy, Fluorescence, Pregnancy, Repressor Proteins, Trophoblasts, Giant Cells, Microscopy, Confocal, Hepatocytes, Microscopy, Electron, Transmission, Chromatin Immunoprecipitation, E2F Transcription Factors, E2F1 Transcription Factor, E2F3 Transcription Factor, E2F7 Transcription Factor, E2F2 Transcription Factor, Mice
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