MAPPING OF CHOLECYSTOKININ TRANSCRIPTION IN TRANSGENIC MOUSE-BRAIN USING ESCHERICHIA-COLI BETA-GALACTOSIDASE REPORTER GENE

Cholecystokinin (CCK), a neuro-gut peptide, occurs not only in the ner vous but also in the digestive system. As a first step in elucidating whether CCK gene expression and its physiological functions co-operate in these separate organs, transgenic mice were produced using CCK pro moter that directs bacterial beta-galactosidase as a reporter gene. A new transgenic vector was constructed, inserting the SV40 poly A signa l 5' to the CCK promoter to impede any transcription upstream of the t ransgene. A 2.4 kb.p. region upstream to the transcription start site of the mouse CCK gene was used as the promoter. Transgene expression w as detected first at embryonic 13.5 days in the central nervous system and increased after birth. The distribution of cells expressing beta- galactosidase transgene agreed fairly well with that of in situ hybrid ization. In addition, the upregulation of CCK gene expression was clea rly demonstrated by expressing beta-galactosidase after injury to the brain. These results indicated that the 2.4 kb.p, of the CCK gene prom oter region was sufficient to direct appropriate tissue-specific gene expression in mice.