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© 1995 Oxford University Press

OTHER

Physical mapping of the Tec and Gabrb1 loci reveals that the Wsh mutation on mouse chromosome 5 is associated with an inversion

Deborah L. Nagle, Christine A. Kozak1, Hiroyuki Mano2, Verne M. Chapman3,{dagger} and Maja Bucan*,

Department of Psychiatry, University of Pennsylvania 415 Curie Boulevard, Philadelphia, PA 19104 1National Institute of Allergy and Infectious Diseases Bethesda, MD 20892, USA 2Department of Molecular Biology, Jichi Medical School Tochigi, Japan 3Department of Molecular and Cellular Biology, Roswell Park Cancer Institute Elm and Carlton Streets, Buffalo, NY 14623, USA

*To whom correspondence should be addressed

Received June 6, 1995; Revised July 24, 1995; Accepted July 24, 1995

In the mouse, mutations in the c-Kit proto-oncogene, a member of the receptor tyrosine kinase (RTK) gene family, have pleiotropic effects on hematopoiesis, pigmentation and fertility (dominant spotting, W). However, in the Wsh allele the defect is confined to abnormal pigmentation caused by the disruption of 5' regulatory sequences of Kit leaving an intact structural gene. In this report, the previously published physical map around the Pdgfra-Kit-Flk1 RTK loci is extended by mapping the loci encoding the GABAA ({gamma}-aminobutyric acid) receptor subunit beta 1, Gabrb1 and a cytoplasmic kinase (Tec) 3 Mb proximal to Kit. PFGE analysis of the wild-type (C57BL/6J) chromosome demonstrates the following gene order: cen-Gabrb1-Tec-Pdgfra-Kit, whereas the analysis of Wsh/Wsh DNA is consistent with the order: cen-Gabrb1-Pdgfra-Tec-Kit. This altered physical map can be explained by an inversion on the Wsh chromosome located proximally to the Kit locus and spanning the 2.8 Mb Pdgfra-Tec chromosomal segment. This high resolution physical mapping study identifies large DNA fragments that span the two inversion breakpoints and potentially carry Kit upstream regulatory elements involved in the control of Kit expression during embryonic development.

{dagger}Deceased August 30, 1995


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