Gene expression profiles in a transgenic animal model of fragile X syndrome

被引:42
作者
D'Agata, V [1 ]
Warren, ST
Zhao, WQ
Torre, ER
Alkon, DL
Cavallaro, S
机构
[1] W Virginia Univ, Blanchette Rockefeller Neurosci Inst, Rockville, MD 20850 USA
[2] Inst Neurol Sci, CNR, I-95123 Catania, Italy
[3] Emory Univ, Sch Med, Howard Hughes Med Inst, Atlanta, GA 30322 USA
[4] Emory Univ, Sch Med, Dept Biochem, Atlanta, GA 30322 USA
[5] Emory Univ, Sch Med, Dept Pediat, Atlanta, GA 30322 USA
[6] Emory Univ, Sch Med, Dept Genet, Atlanta, GA 30322 USA
关键词
D O I
10.1006/nbdi.2002.0506
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Fragile X syndrome is the most common inherited form of mental retardation. Although this syndrome originates from the absence of the RNA-binding protein FMRP, the molecular mechanisms underlying the cognitive deficits are unknown. The expression pattern of 6789 genes was studied in the brains of wild-type and FMR1 knockout mice, a fragile X syndrome animal model that has been associated with cognitive deficits. Differential expression of more than two-fold was observed for the brain mRNA levels of 73 genes. Differential expression of nine of these genes was confirmed by real-time quantitative reverse transcription-polymerase chain reaction and by in situ hybridization. In addition to corroborating the microarray data, the in situ hybridization analysis showed distinct spatial distribution patterns of microtubule-associated protein 2 and amyloid beta precursor protein. A number of differentially expressed genes associated with the fragile X syndrome phenotype have been previously involved in other memory or cognitive disorders. (C) 2002 Elsevier Science (USA).
引用
收藏
页码:211 / 218
页数:8
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