Permanent URL to this publication: http://dx.doi.org/10.5167/uzh-1875
Hergersberg, M; Matsuo, K; Gassmann, M; Schaffner, W; Lüscher, B; Rülicke, T; Aguzzi, A (1995). Tissue-specific expression of a FMR1/beta-galactosidase fusion gene in transgenic mice. Human Molecular Genetics, 4(3):359-366.
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 beta-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.
|Item Type:||Journal Article, refereed|
|Communities & Collections:||04 Faculty of Medicine > University Hospital Zurich > Institute of Neuropathology|
|DDC:||570 Life sciences; biology|
610 Medicine & health
|Date:||1 March 1995|
|Deposited On:||11 Feb 2008 12:26|
|Last Modified:||24 Dec 2013 15:34|
|Publisher:||Oxford University Press|
|Citations:||Web of Science®. Times Cited: 56|
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