The RET proto-oncogene is involved in the development of both kidney and ne
ural crests derived tissues. RET deleterious mutations cause hereditary neu
roendocrine tumours and congenital intestinal aganglionosis. Ongoing effort
s aimed at elucidating the function of this gene include expression studies
in different species and in transgenic mice. As first step in the study of
Rct expression in mouse, we obtained the mouse Ret genomic structure. Intr
on-exon boundaries were determined and sequenced, all introns, but the firs
t one were amplified and cloned, and exons positioned in a restriction map.
Mouse and human genes comparison indicates a highly conserved genomic orga
nisation, except for exon 21 which is not conserved in mouse. A region exte
nding 386 bp 5 ' to the first exon was sequenced and compared with its huma
n counterpart. Some features, reported for the human promoter, like the abs
ence of TATA or CAAT boxes and a high GC content, are conserved.