Partial leptin receptor gene deletion in transgenic mice prevents expression of the membrane-bound isoforms except for Ob-Rc.
Examination of random insertional mutations in transgenic animals harbouring an abnormal phenotype contributes to the discovery of new genes and/or the understanding of already known genes. Here we describe a transgenic mouse line showing early-onset obesity as consequence of the transgene insertion. Molecular genetic analysis revealed a partial deletion of the leptin receptor (Lepr, Ob-R) gene including the coding sequences downstream of exon 17'. This defect prevents the expression of all described membrane-bound isoforms of Ob-R except for isoform Ob-Rc in the homozygous transgenic animals. Thus, this mouse model might be useful for the investigation of the function of the short Ob-R isoforms.
Reichart
U
U
Institut für Tierzucht und Genetik, Veterinärmedizinische Universität Wien, Veterinärplatz 1, Vienna, A-1210, Austria.
Kappler
R
R
Scherthan
H
H
Wolf
E
E
Müller
M
M
Brem
G
G
Aigner
B
B
D000818:Animals; D002352:Carrier Proteins / Q000235:genetics*; D017353:Gene Deletion; D020738:Leptin / Q000235:genetics*; D051379:Mice; D008822:Mice, Transgenic; D016254:Mutagenesis, Insertional; D020033:Protein Isoforms / Q000235:genetics*; D012333:RNA, Messenger / Q000235:genetics; D011956:Receptors, Cell Surface; D054411:Receptors, Leptin; D019076:Transgenes
D002352:Carrier Proteins; D020738:Leptin; D020033:Protein Isoforms; D012333:RNA, Messenger; D011956:Receptors, Cell Surface; D054411:Receptors, Leptin; C515447:leptin receptor, mouse