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Tissue-Specific, Hormonal, and Developmental Regulation of SCC-LacZ Expression in Transgenic Mice Leads to Adrenocortical Zone Characterization¹

Institute of Molecular Biology, Academia Sinica (M.-C.H., S.-J.C., Y.-Y.H., N.-C.H., H.L., C.-c.C.); Institute of Life Sciences, National Defense Medical Center (M.-C.H.); and the Division of Endocrinology and Metabolism, Chang-Gung Memorial Hospital Medical Center (Y.-Y.H.), Taipei, Taiwan 11529, Republic of China

Address all correspondence and requests for reprints to: Dr. Bon-chu Chung, Institute of Molecular Biology, Academia Sinica, Nankang, Taipei, Taiwan 11529, Republic of China. E-mail: mbchung{at}sinica.edu.tw

We report here the study of the human CYP11A1 promoter in driving tissue-specific, developmentally and hormonally regulated reporter gene expression. A 4.4-kb fragment containing all known regulatory elements is more efficient than a short basal promoter fused to an upstream adrenal enhancer in driving reporter LacZ gene expression both in cell culture and in transgenic mice. The LacZ gene controlled by the 4.4- and 2.3-kb promoters was expressed in the adrenal cortex, testicular Leydig cells, ovarian corpora lutea, and granulosa cells. Transgene expression in the adrenals was stimulated by ACTH, indicating the presence of ACTH-responsive sequence. ß-Galactosidase activity was first detected in the adrenal primordia at 11.5 days postcoitum. Its expression continued throughout all stages of adrenal development in a pattern similar to that of the endogenous CYP11A1, which was expressed in all zones of the adrenal cortex, but was strongest in the X zone. The X zone grew before puberty but regressed afterward, as did the levels of CYP11A1 and LacZ gene expression in the X zone. Our study of the CYP11A1 promoter in transgenic mice led to characterization of the adrenocortical zones.

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