© 1995 Oxford University Press
RESEARCH-ARTICLE |
Tissue-specific expression of a FMR1/ß-galactosidase fusion gene in transgenic mice
Institut für Medizinische Genetik, Universität Zürich Rämistr, 74, CH-8001 Zürich 1Institut für Molekularbiologie II, Universität Zürich Winterthurerstr, 190, CH-8057 Zürich, Switzerland 2Physiologisches Institut, Universität Zürich Winterthurerstr. 190, CH-8057 Zürich, Switzerland 3Pharmakologisches Institut, Universität Zürich Winterthurerstr. 190, CH-8057 Zürich, Switzerland 4Biologisches Zentrallabor, Universitätsspital Zürich Sternwartstr. 6, CH-8091 Zürich, Switzerland 5Institut für Neuropathologie, Universitätsspital Zürich Schmelzbergstr. 12, CH-8091 Zürich, Switzerland
*To whom correspondence should be addressed
Received October 12, 1994; Revised December 19, 1994; Accepted December 19, 1994
Fragile X syndrome is one of the most common genetic causes of mental retardation, yet the mechanisms controlling expression of the fragile X mental retardation gene FMR1 are poorly understood. To identify sequences regulating FMR1 transcription, transgenic mouse lines were established using a fusion gene consisting of an E.coli ß-galactosidase reporter gene (lacZ) linked to a 2.8 kb fragment spanning the 5'-region of FMR1. Five transgenic mouse lines showed lacZ expression in brain, in particular in neurons of the hippocampus and the granular layer of the cerebellum. Expression of the reporter gene was also detected in Leydig cells and spermatogonia in the testis, in many epithelia of adult mice, and in the two other steroidogenic cell types, adrenal cortex cells and ovarian follicle cells. Embryonic tissues which showed strong activity of the reporter gene included the telencephalon, the genital ridge, and the notochord. This expression pattern closely resembles the endogenous one, indicating that the 5' FMR1 gene promoter region used in this study contains most cis-acting elements regulating FMR1 transcription.
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