Tissue-specific expression of a FMR1/β-galactosidase fusion gene in transgenic mice

Martin Hergersberg, Koichi Matsuo, Max Gassmann, Walter Schaffner, Bernhard Lüscher, Thomas Rülicke, Adriano Aguzzi

研究成果: Article査読

66 被引用数 (Scopus)

抄録

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 β-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. / 1995 Oxford University Press.

本文言語English
ページ(範囲)359-366
ページ数8
ジャーナルHuman molecular genetics
4
3
DOI
出版ステータスPublished - 1995 3月
外部発表はい

ASJC Scopus subject areas

  • 分子生物学
  • 遺伝学
  • 遺伝学(臨床)

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