An Ovol2-Zeb1 Transcriptional Circuit Regulates Epithelial Directional Migration and Proliferation

November 2018 in “ EMBO Reports ”

Daniel Haensel, Peng Sun, Adam L. MacLean, Xianghui Ma, Yuan Zhou, Marc P. Stemmler, Simone Brabletz, Geert Berx, Maksim V. Plikus, Qing Nie, Thomas Brabletz, Xing Dai

Ovol2 Zeb1 epithelial cell migration epithelial cell proliferation wound healing hair follicle regeneration epidermal cell migration epidermal cell proliferation matrix cell proliferation matrix cell differentiation epithelial-to-mesenchymal transition EMT epidermal keratinocytes bulge hair follicle stem cells Bu-HFSCs post-mitotic cell cycle arrest

TLDR The Ovol2-Zeb1 circuit is crucial for skin healing and hair growth by guiding cell movement and growth.

The document details a study investigating the role of the Ovol2-Zeb1 transcriptional circuit in skin regeneration and repair, focusing on its impact on epithelial cell migration and proliferation. Ovol2, a transcriptional repressor, was found to be essential for proper wound healing and hair follicle regeneration in mice. Ovol2-deficient mice showed impaired wound healing due to abnormal epidermal cell migration and proliferation, as well as delayed hair follicle regeneration with defects in matrix cell proliferation and differentiation. The study also demonstrated that Ovol2 deficiency led to enhanced epithelial-to-mesenchymal transition (EMT) and reduced proliferation in epidermal keratinocytes and bulge hair follicle stem cells (Bu-HFSCs), with increased migration speed but less directionality and a post-mitotic cell cycle arrest. Deleting Zeb1, an EMT-promoting factor, in Ovol2-deficient Bu-HFSCs restored their directional migration. These findings emphasize the critical role of the Ovol2-Zeb1 circuit in controlling the directional migration and proliferation of epithelial stem and progenitor cells for effective skin regeneration and repair. However, the number of mice used in the study was not specified, which is important for evaluating the study's strength.

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