Figures
Claudin 1, Ecadherin and keratin 14 in the tail skin of a mouse.
In this issue of PLOS Genetics, DiTommaso et al. describe the phenotype of mice carrying inactivating mutations in Keratin 76 (Krt76), highlighting the gene as indispensable for skin barrier function and cutaneous wound healing. They also describe a role for KRT76 in maintaining the function of intercellular tight junctions, where it is required for normal CLAUDIN1 localisation. This work supports an emerging body of evidence which challenges the classical view of the keratins as simple structural proteins. Image: Claudin 1 (green), Ecadherin (red) and keratin 14 (blue) in the tail skin of a mouse. See DiTommaso et al.
Image Credit: Tia DiTommaso
Citation: (2014) PLoS Genetics Issue Image | Vol. 10(10) October 2014. PLoS Genet 10(10): ev10.i10. https://doi.org/10.1371/image.pgen.v10.i10
Published: October 30, 2014
Copyright: © 2014 DiTommaso et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
In this issue of PLOS Genetics, DiTommaso et al. describe the phenotype of mice carrying inactivating mutations in Keratin 76 (Krt76), highlighting the gene as indispensable for skin barrier function and cutaneous wound healing. They also describe a role for KRT76 in maintaining the function of intercellular tight junctions, where it is required for normal CLAUDIN1 localisation. This work supports an emerging body of evidence which challenges the classical view of the keratins as simple structural proteins. Image: Claudin 1 (green), Ecadherin (red) and keratin 14 (blue) in the tail skin of a mouse. See DiTommaso et al.
Image Credit: Tia DiTommaso