Mammalian Genome 9, 780–781 (1998). Incorporating Mouse Genome © Springer-Verlag New York Inc. 1998 db-Pas Partial duplication in the Lepr mutation is a result of unequal crossing over Shun Mei Liu, Rudolph L. Leibel, Streamson C. Chua, Jr. Division of Molecular Genetics, Department of Pediatrics, Columbia University College of Physicians and Surgeons, Russ Berrie Medical Sciences Pavilion, 1150 St. Nicholas Avenue, Box 110, New York, New York 10032, USA Received: 2 March 1998 / Accepted: 15 May 1998 The leptin receptor gene (Lepr) has multiple splice variants, com- sizes (2 kbp) were amplified from both types of mice. The frag- prising at least five isoforms that have different signal transduction ment amplified from a wild-type DW/Pas mouse was sequenced and putative binding/transport capabilities (Lee et al. 1996; Tarta- with primer NewR1. A portion of this fragment showed perfect glia et al. 1995; Chua et al. 1997). A molecular analysis of the homology to the segment 38 of coding exon 6 of the Ex5L ﬁ Ex4L functions of the various Lepr isoforms will require information fragment from the db-Pas mice. This indicates that the segment regarding the molecular nature of various spontaneous mutations that interrupts coding exon 6 in the
Mammalian Genome – Springer Journals
Published: Sep 1, 1998
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