Generating LacZ-reporter transgenic mice to identify α1 (XIX) Collagen (Col19a1) expression in Dermal Papilla Cells

Document Type : Original Article

Authors

1 Laboratory of Molecular Design and Synthesis, Department of Regenerative Medicine and Applied Medical Sciences, Graduate School of Medicine, Gifu University

2 Department of Anatomy and Embryology, Faculty of Veterinary Medicine, Benha University, Moshtohor, Toukh 13736, Egypt

3 Laboratory of Molecular Design and Synthesis, Department of Regenerative Medicine and Applied Medical Sciences, Graduate School of Medicine, Gifu University, 1-1 Yanagido, Gifu 501-1194, Japan.

4 Laboratory of Molecular Design and Synthesis, Department of Regenerative Medicine and Applied Medical Sciences, Graduate School of Medicine, Gifu University, 1-1 Yanagido, Gifu 501-1194, Japan

5 Department of Anatomy and Embryology, Faculty of Veterinary Medicine, Kafr Elsheikh University, Kafr Elsheikh 33516, Egypt

Abstract

It is widely accepted the concept that tissue morphogenesis is mediated by reciprocal interactions
between epithelial and mesenchymal cells, whereas the molecular details of these interactions remain
largely elusive. The hair follicle (HF) is a mini-organ whose proper morphogenesis is governed by a
series of interactions between epidermal and dermal cells. Due to its relatively simple structure, the HF
affords an excellent model to decipher the molecular mechanisms of epithelial – mesenchymal
interactions. To explore the molecular mechanisms by which Dermal Papilla (DP) cells regulate hair
follicle formation, we performed a comparative transcriptome analysis and identified numerous genes
preferentially expressed in the DP cells. Among these, a gene encoding type XIX Collagen (Col19a1)
has become the focus of our attention because of its extensive evolutionary conservation. We generated
Col19a1LacZ reporter mice using CRISPR/Cas9 system to induce homologous recombination to
recapitulate Col19a1 expression pattern. In mouse embryos, Col19a1LacZ expression is confined to the
DP cells of hair follicles, ring sinus of whiskers, skeletal muscles and basal keratinocyte layer of skin
epidermis of limbs and tail. Moreover, Col19LacZ started to be expressed at E14.5 in the dermal
condensates of hair germ stage to the DP cells of mature hair follicle but not in the placode stage.
Ongoing generation of Col19a1 null mice will ultimately explore the functional role of Col19a1 during
HF morphogenesis. From this perspective, it is plausible to expect that future studies will provide
additional functional evidence for Col19a1 during development which might be a useful tool to
understand the molecular mechanisms undergoing HF stem cell regulation

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