# TMEM207-mediated the impairment of skin regeneration through YAP sequestration in an allergic contact dermatitis model

## TL;DR

This study shows that abnormal TMEM207 expression impairs skin regeneration by affecting YAP, worsening allergic contact dermatitis.

## Contribution

The novel finding is that TMEM207 interacts with YAP to impair skin regeneration in an allergic dermatitis model.

## Key findings

- TMEM207 is expressed in sebaceous glands and hair follicles in mice.
- TMEM207 binds to YAP, reducing its nuclear localization.
- Abnormal TMEM207 expression decreases skin regeneration and worsens dermatitis.

## Abstract

The Yes-associated protein (YAP) family of transcriptional coactivators has emerged as a potent promoter of cell proliferation in many types of stem/progenitor cells and cancers. Skin is a squamous epithelium that is continuously regenerated by stem/progenitor cells in the basal layer and is capable of wound healing, and YAP also plays an important role in maintaining skin homeostasis and cellular proliferation. Therefore, we focused on YAP and investigated the importance of YAP regulation in allergic contact dermatitis from the perspective of wound healing and regeneration.

We investigated the expression and pathological characteristics of Transmembrane protein 207 (TMEM207), focusing on YAP-mediated regulation in atopic models, as abnormal TMEM207 expression may cause various functional abnormalities or regulate the function of YAP.

TMEM207 was detected not only in the stomach and large intestine but also in the bulge region of the sebaceous glands and hair roots in mice expressing TMEM207. In addition, ATP binding cassette subfamily B member 1 (ABCB1) expression decreased in the sebaceous glands, and MIB E3 Ubiquitin Protein Ligase 1 (MIB-1) expression diminished in the epidermis. Furthermore, although we were unable to confirm the binding of TMEM207 to NEDD4, we confirmed the binding of TMEM207 to the Yes1-associated transcription factor (YAP) by immunoprecipitation, and a decrease in the nuclear localization of YAP was observed by immunohistochemical staining.

Our findings indicate that abnormal expression of TMEM207 is involved in the decline of skin regeneration capacity through YAP, leading to the aggravation of Allergic contact dermatitis.

•TMEM207 was detected in the sebaceous glands and the bulge region of hair follicle in mice expressing TMEM207.•MIB-1 expression was decreased in the epidermis in mice expressing TMEM207.•Although TMEM207 does not bind to NEDD4, the binding of TMEM207 to YAP was confirmed by immunoprecipitation.•Abnormal expression of TMEM207 is involved in the skin regeneration capacity via YAP.

TMEM207 was detected in the sebaceous glands and the bulge region of hair follicle in mice expressing TMEM207.

MIB-1 expression was decreased in the epidermis in mice expressing TMEM207.

Although TMEM207 does not bind to NEDD4, the binding of TMEM207 to YAP was confirmed by immunoprecipitation.

Abnormal expression of TMEM207 is involved in the skin regeneration capacity via YAP.