# Specific In Vivo Ablation of Lrig1-Positive Follicular Progenitor Cells Results in Sebaceous Gland Loss in Mice

## TL;DR

Deleting Lrig1-positive cells in mice leads to temporary loss of sebaceous glands, showing their key role in gland formation and maintenance.

## Contribution

Demonstrates the essential role of Lrig1-positive progenitor cells in sebaceous gland homeostasis through in vivo ablation.

## Key findings

- Selective depletion of Lrig1-positive cells caused complete but reversible sebaceous gland loss in mice.
- Without Lrig1 cells, junctional-zone keratinocytes adopted an epidermis-like phenotype and failed to form sebocytes.
- Sebaceous gland recovery occurred after six months following cell depletion.

## Abstract

Leucine-rich repeats and immunoglobulin-like domains protein 1 (Lrig1) is a functional inhibitor of the epidermal growth factor receptor. Lrig1-positive stem cells are located in the isthmus region of the mouse hair follicle (HF) and are known contributors to sebaceous gland (SG) formation and homeostasis. In this study, we performed a topical tamoxifen inducible diphtheria toxin-mediated ablation of Lrig1-expressing cells in transgenic mice to investigate their function in vivo. Selective depletion of Lrig1-positive cells resulted in a complete but reversible loss of SGs, with atrophy beginning at day 14 and full recovery occurring after six months. In the absence of the Lrig1 niche, junctional-zone keratinocytes adopted an interfollicular epidermis-like phenotype (K1-positive), and repopulating cells from other epidermal compartments failed to differentiate into the sebocyte lineage. These findings demonstrate that Lrig1-positive progenitors are crucial for proper sebaceous gland morphogenesis and maintenance. Our results highlight the importance of Lrig1-positive cells in SG-related skin physiology.