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

Qi Miao (), Matthew C. Hill, Fengju Chen, Qianxing Mo, Amy T. Ku, Carlos Ramos, Elisabeth Sock, Véronique Lefebvre and Hoang Nguyen ()
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Qi Miao: Baylor College of Medicine
Matthew C. Hill: Baylor College of Medicine
Fengju Chen: Baylor College of Medicine
Qianxing Mo: Baylor College of Medicine
Amy T. Ku: Baylor College of Medicine
Carlos Ramos: Baylor College of Medicine
Elisabeth Sock: Friedrich-Alexander-Universität Erlangen-Nürnberg
Véronique Lefebvre: Children’s Hospital of Philadelphia
Hoang Nguyen: Baylor College of Medicine

Nature Communications, 2019, vol. 10, issue 1, 1-20

Abstract: 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.

Date: 2019
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DOI: 10.1038/s41467-019-11880-9

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