posted on 2016-11-07, 15:12authored byEmmanuel Debrand, Francesco J. Conti, Neil Bate, Lorraine Spence, Daniela Mazzeo, Catrin A. Pritchard, Susan J. Monkley, David R. Critchley
Mice homozygous for several Tln2 gene targeted alleles are viable and fertile. Here we show that although the expression of talin2 protein is drastically reduced in muscle from these mice, other tissues continue to express talin2 albeit at reduced levels. We therefore generated a Tln2 allele lacking the entire coding sequence (Tln2(cd)). Tln2(cd/cd) mice were viable and fertile, and the genotypes of Tln2(cd/+) intercrosses were at the expected Mendelian ratio. Tln2(cd/cd) mice showed no major difference in body mass or the weight of the major organs compared to wild-type, although they displayed a mildly dystrophic phenotype. Moreover, Tln2(cd/cd) mouse embryo fibroblasts showed no obvious defects in cell adhesion, migration or proliferation. However, the number of Tln2(cd/cd) pups surviving to adulthood was variable suggesting that such mice have an underlying defect.
Funding
The Wellcome Trust and Cancer Research UK supported this work.
History
Citation
Biochemical and Biophysical Research Communications , 2012, 426 (2), pp. 190-195
Author affiliation
/Organisation/COLLEGE OF MEDICINE, BIOLOGICAL SCIENCES AND PSYCHOLOGY/School of Medicine/Department of Cancer Studies and Molecular Medicine
Version
VoR (Version of Record)
Published in
Biochemical and Biophysical Research Communications