Novel Roles for SUMOylation in Cellular Plasticity

Bruno Di Stefano¹, Konrad Hochedlinger²

Affiliations

¹ Department of Molecular Biology, Massachusetts General Hospital, Harvard Medical School, 185 Cambridge Street, Boston, MA 02114, USA; Center for Regenerative Medicine, Massachusetts General Hospital, Harvard Medical School, 185 Cambridge Street, Boston, MA 02114, USA; Cancer Center, Massachusetts General Hospital, Harvard Medical School, 185 Cambridge Street, Boston, MA 02114, USA; Department of Stem Cell and Regenerative Biology, Harvard University, Cambridge, MA 02138, USA; Harvard Stem Cell Institute, 1350 Massachusetts Avenue, Cambridge, MA 02138, USA.
² Department of Molecular Biology, Massachusetts General Hospital, Harvard Medical School, 185 Cambridge Street, Boston, MA 02114, USA; Center for Regenerative Medicine, Massachusetts General Hospital, Harvard Medical School, 185 Cambridge Street, Boston, MA 02114, USA; Cancer Center, Massachusetts General Hospital, Harvard Medical School, 185 Cambridge Street, Boston, MA 02114, USA; Department of Stem Cell and Regenerative Biology, Harvard University, Cambridge, MA 02138, USA; Harvard Stem Cell Institute, 1350 Massachusetts Avenue, Cambridge, MA 02138, USA. Electronic address: khochedlinger@mgh.harvard.edu.

PMID: 30463679
PMCID: PMC6456908
DOI: 10.1016/j.tcb.2018.10.001

Comment

Novel Roles for SUMOylation in Cellular Plasticity

Bruno Di Stefano et al. Trends Cell Biol. 2018 Dec.

. 2018 Dec;28(12):971-973.

doi: 10.1016/j.tcb.2018.10.001. Epub 2018 Oct 26.

Authors

Bruno Di Stefano¹, Konrad Hochedlinger²

Affiliations

¹ Department of Molecular Biology, Massachusetts General Hospital, Harvard Medical School, 185 Cambridge Street, Boston, MA 02114, USA; Center for Regenerative Medicine, Massachusetts General Hospital, Harvard Medical School, 185 Cambridge Street, Boston, MA 02114, USA; Cancer Center, Massachusetts General Hospital, Harvard Medical School, 185 Cambridge Street, Boston, MA 02114, USA; Department of Stem Cell and Regenerative Biology, Harvard University, Cambridge, MA 02138, USA; Harvard Stem Cell Institute, 1350 Massachusetts Avenue, Cambridge, MA 02138, USA.
² Department of Molecular Biology, Massachusetts General Hospital, Harvard Medical School, 185 Cambridge Street, Boston, MA 02114, USA; Center for Regenerative Medicine, Massachusetts General Hospital, Harvard Medical School, 185 Cambridge Street, Boston, MA 02114, USA; Cancer Center, Massachusetts General Hospital, Harvard Medical School, 185 Cambridge Street, Boston, MA 02114, USA; Department of Stem Cell and Regenerative Biology, Harvard University, Cambridge, MA 02138, USA; Harvard Stem Cell Institute, 1350 Massachusetts Avenue, Cambridge, MA 02138, USA. Electronic address: khochedlinger@mgh.harvard.edu.

PMID: 30463679
PMCID: PMC6456908
DOI: 10.1016/j.tcb.2018.10.001

Abstract

Cell fate transitions involve rapid changes in gene expression patterns, yet the role of post-translational modifications in these processes remains underexplored. A recent study identifies SUMOylation as a guardian of cell identity that acts during differentiation and reprogramming by reinforcing active enhancers and maintaining silenced heterochromatin in a context-specific manner.

PubMed Disclaimer

Figures

**Figure 1.. Roles of SUMOylation in controlling cellular and chromatin plasticity.**
(A) Hyposumoylation facilitates the reprogramming of mouse embryonic fibroblasts (MEFs) into iPSCs and the conversion of ESCs to 2C-like cells. (B) SUMO suppression facilitates cell fate change in different cellular systems with or without ectopic expression of transcription factors. (C) SUMO influences enhancer activity and heterochromatin levels. In MEFs, SUMO facilitates the cooperative binding of somatic TFs at enhancers. In ESCs, SUMOylation of components of the PRC1.6 complex and of heterochromatic factors such as SETDB1, HP1α and KAP1 contributes to the silencing of ERV-associated genes.

See this image and copyright information in PMC

Comment on

SUMO Safeguards Somatic and Pluripotent Cell Identities by Enforcing Distinct Chromatin States.
Cossec JC, Theurillat I, Chica C, Búa Aguín S, Gaume X, Andrieux A, Iturbide A, Jouvion G, Li H, Bossis G, Seeler JS, Torres-Padilla ME, Dejean A. Cossec JC, et al. Cell Stem Cell. 2018 Nov 1;23(5):742-757.e8. doi: 10.1016/j.stem.2018.10.001. Epub 2018 Oct 25. Cell Stem Cell. 2018. PMID: 30401455

References

1. Deribe YL et al. (2010) Post-translational modifications in signal integration. Nat Struct Mol Biol 17 (6), 666–72. - PubMed
1. Flotho A and Melchior F (2013) Sumoylation: a regulatory protein modification in health and disease. Annu Rev Biochem 82, 357–85. - PubMed
1. Wang L et al. (2014) SUMO2 is essential while SUMO3 is dispensable for mouse embryonic development. EMBO Rep 15 (8), 878–85. - PMC - PubMed
1. Borkent M et al. (2016) A Serial shRNA Screen for Roadblocks to Reprogramming Identifies the Protein Modifier SUMO2. Stem Cell Reports 6 (5), 704–716. - PMC - PubMed
1. Cossec J et al. (2018) SUMO safeguards somatic and pluripotent cell identities by enforcing distinct chromatin states. Cell Stem Cell. - PubMed

Publication types

Actions

MeSH terms

Actions
Actions
Actions
Actions
Actions

Save citation to file

Email citation

Add to Collections

Add to My Bibliography

Your saved search

Create a file for external citation management software

Your RSS Feed

Novel Roles for SUMOylation in Cellular Plasticity

Affiliations

Novel Roles for SUMOylation in Cellular Plasticity

Authors

Affiliations

Abstract

Figures

Comment on

References

Publication types

MeSH terms

Substances

Grants and funding

LinkOut - more resources

Full Text Sources