SOX11 and SOX4 drive the reactivation of an embryonic gene program during murine wound repair

Miao Q, Hill MC, Chen F, Mo Q, Ku AT, Ramos C, Sock E, Lefebvre V, Nguyen H (2019)

Publication Type: Journal article

Publication year: 2019

Journal

Nature Communications Nature Publishing Group: Nature Communications

Book Volume: 10

Article Number: 4042

Journal Issue: 1

DOI: 10.1038/s41467-019-11880-9

Abstract

Tissue injury induces changes in cellular identity, but the underlying molecular mechanisms remain obscure. Here, we show that upon damage in a mouse model, epidermal cells at the wound edge convert to an embryonic-like state, altering particularly the cytoskeletal/extracellular matrix (ECM) components and differentiation program. We show that SOX11 and its closest relative SOX4 dictate embryonic epidermal state, regulating genes involved in epidermal development as well as cytoskeletal/ECM organization. Correspondingly, postnatal induction of SOX11 represses epidermal terminal differentiation while deficiency of Sox11 and Sox4 accelerates differentiation and dramatically impairs cell motility and re-epithelialization. Amongst the embryonic genes reactivated at the wound edge, we identify fascin actin-bundling protein 1 (FSCN1) as a critical direct target of SOX11 and SOX4 regulating cell migration. Our study identifies the reactivated embryonic gene program during wound repair and demonstrates that SOX11 and SOX4 play a central role in this process.

Authors with CRIS profile

Elisabeth Sock Lehrstuhl für Biochemie und Pathobiochemie

Involved external institutions

Baylor College of Medicine US United States (USA) (US) Children's Hospital of Philadelphia US United States (USA) (US)

How to cite

APA:

Miao, Q., Hill, M.C., Chen, F., Mo, Q., Ku, A.T., Ramos, C.,... Nguyen, H. (2019). SOX11 and SOX4 drive the reactivation of an embryonic gene program during murine wound repair. Nature Communications, 10(1). https://dx.doi.org/10.1038/s41467-019-11880-9

MLA:

Miao, Qi, et al. "SOX11 and SOX4 drive the reactivation of an embryonic gene program during murine wound repair." Nature Communications 10.1 (2019).

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