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FISH mapping of the mouse Ret oncogene to the junction of G-bands E3/F1 on Chromosome 6 indicates a need for reassessment of the physical and consensus maps

The RET proto-oncogene encodes a cell-surface glycoprotein with cytoplasmic tyrosine kinase activity (Takahashi et al., 1989). Mutations in RET have been associated with four human disease syndromes: Hirschprung’s disease, familial medullary thyroid carcinoma, and two forms of multiple endocrine neoplasia, type 2A and 2B (van Heyningen, 1994). The mouse Ret gene has been cloned (Iwamoto et al., 1993) and is expressed in normal mouse spinal cord and in Fas and Fas1 lymphadenopathy (Takahashi et al., 1988). Mice homozygous for the targeted knockout of Ret develop to term, but die soon after birth with renal agenesis/dysgenesis (Schuchardt et al., 1995). They also lack enteric neurons throughout the digestive tract. Thus the Ret gene product may be a receptor for a factor involved in development of a number of neural cell lineages, and in kidney organogenesis (Pachnis et al., 1993). Ret was assigned by interspecific backcross analysis to 53.2 cM on Chr 6, 1.1 cM distal to Raf1 (Elliott and Moore 1998, Li et al., 1995). The mapping of loci in this region on the physical map appears contradictory in that Raf1 has been positioned in G-band 6C3 by in situ hybridisation (Tailor and Martin-DeLeon, 1989), but Pparg and Sdf1, only 0.5 cM distal to Raf1 on the consensus map, have been assigned by FISH to bands E3/ F1 and F1 respectively (Zhu et al., 1995, Nomura et al., 1996). The close linkage of these loci is incompatible with these alleged G-band locations since, according to the Mouse Chromosome Atlas (Lyon and Kirby, 1996), G-bands 6C3 and F1 could be up to 10 cM apart. Del(6)Ums26H (hereafter referred to as Del(6)Ums) is a deletion mutant found by screening progeny of spermatogonially X-irradiated male mice, carriers having umbrous coats, low viability and small body size (Cattanach et al., 1993 ). The deleted chromosome segment of Chr 6 was initially thought to include all of G-band C3. If the FISH assignment of Raf1 to C3 is correct then the Ret locus may be located within the deleted region, or at either of its two breakpoints. If this is the case, mice carrying the Del(6)Ums deletion could provide potential haplo-insufficient models for the human disease syndromes associated with mutations at the RET locus. Therefore, to determine the unequivocal location of the mouse homologue within or outside the deletion Del(6)Ums, and to resolve the existing ambiguity caused by the in situ and FISH mapping of loci in this region, we have positioned Ret directly by FISH using mitotic cells from Del(6)Ums heterozygous mice, carrying both a deleted and normal Chr 6.