The loss of full-length dystrophin from skeletal muscle leads to the clinic
al features of Duchenne muscular dystrophy. Both Dp71, a C-terminal dystrop
hin isoform, and the dystrophin-related protein, utrophin, are present at h
igh levels in many nonmuscle tissues. To investigate the roles of these pro
teins in nonmuscle tissues, mice were generated null for utrophin, and defi
cient in all dystrophin isoforms. These mice reach adulthood and do not app
ear to have any devastating pathology in nonmuscle tissues. (C) 1999 John W
iley & Sons, Inc.