| First Author | Leclerc EA | Year | 2014 |
| Journal | J Cell Sci | Volume | 127 |
| Issue | Pt 13 | Pages | 2862-72 |
| PubMed ID | 24794495 | Mgi Jnum | J:214662 |
| Mgi Id | MGI:5603671 | Doi | 10.1242/jcs.144808 |
| Citation | Leclerc EA, et al. (2014) Mice deficient for the epidermal dermokine beta and gamma isoforms display transient cornification defects. J Cell Sci 127(Pt 13):2862-72 |
| abstractText | Expression of the human dermokine gene (DMKN) leads to the production of four dermokine isoform families. The secreted alpha, beta and gamma isoforms have an epidermis-restricted expression pattern, with Dmkn beta and gamma being specifically expressed by the granular keratinocytes. The delta isoforms are intracellular and ubiquitous. Here, we performed an in-depth characterization of Dmkn expression in mouse skin and found an expression pattern that was less complex than in humans. In particular, mRNA coding for the delta family were absent. Homozygous mice null for the Dmkn beta and gamma isoforms had no obvious phenotype but only a temporary scaly skin during the first week of life. The pups null for the Dmkn beta and gamma isoforms had smaller keratohyalin granules and their cornified envelopes were more sensitive to mechanical stress. At the molecular level, amounts of profilaggrin and filaggrin monomers were reduced whereas amino acid components of the natural moisturizing factor were increased. In addition, the electrophoretic mobility of involucrin was modified, suggesting post-translational modifications. Finally, the mice null for the Dmkn beta and gamma isoforms strongly overexpressed Dmkn alpha. These data are evocative of compensatory mechanisms relevant to the temporary phenotype. Overall, we improved the knowledge of Dmkn expression in mouse and highlighted a role for Dmkn beta and gamma in cornification. |
