Open AccessGeneration and Characterisation of Keratin 7 (K7) Knockout Mice
Author(s) -
Aileen Sandilands,
Frances J.D. Smith,
Declan P. Lunny,
Linda Campbell,
Kirsty M. Davidson,
Stephanie F. MacCallum,
Laura D. Corden,
Lesley Christie,
Stewart Fleming,
E. Birgitte Lane,
W.H. Irwin McLean
Publication year - 2013
Publication title -
plos one
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.99
H-Index - 332
ISSN - 1932-6203
DOI - 10.1371/journal.pone.0064404
Subject(s) - urothelium , keratin , keratin 14 , knockout mouse , keratin 5 , biology , western blot , immunofluorescence , microbiology and biotechnology , keratin 8 , gene expression , embryonic stem cell , gene , genetics , transgene , genetically modified mouse , endocrinology , urinary system , antibody
Keratin 7 (K7) is a Type II member of the keratin superfamily and despite its widespread expression in different types of simple and transitional epithelia, its functional role in vivo remains elusive, in part due to the lack of any appropriate mouse models or any human diseases that are associated with KRT7 gene mutations. Using conventional gene targeting in mouse embryonic stem cells, we report here the generation and characterisation of the first K7 knockout mouse. Loss of K7 led to increased proliferation of the bladder urothelium although this was not associated with hyperplasia. K18, a presumptive type I assembly partner for K7, showed reduced expression in the bladder whereas K20, a marker of the terminally differentiated superficial urothelial cells was transcriptionally up-regulated. No other epithelia were seen to be adversely affected by the loss of K7 and western blot and immunofluorescence microscopy analysis revealed that the expression of K8, K18, K19 and K20 were not altered in the absence of K7, with the exception of the kidney where there was reduced K18 expression.