Gonadal function is critically dependant on regulated secretion of the 
gonadotropin hormones from anterior pituitary gonadotroph cells. Gonadotropin 
biosynthesis and release is triggered by the binding of hypothalamic GnRH to 
GnRH receptor expressed on the gonadotroph cell surface. The repertoire of 
regulatory molecules involved in this process are still being defined. We used 
the mouse L beta T2 gonadotroph cell line, which expresses both gonadotropin 
hormones, as a model to investigate GnRH regulation of gene expression and 
differential display reverse transcription-polymerase chain reaction (RT-PCR) to 
identify and isolate hormonally induced changes. This approach identified 
Fanconi anemia a (Fanca), a gene implicated in DNA damage repair, as a 
differentially expressed transcript. Mutations in Fanca account for the majority 
of cases of Fanconi anemia (FA), a recessively inherited disease identified by 
congenital defects, bone marrow failure, infertility, and cancer susceptibility. 
We confirmed expression and hormonal regulation of Fanca mRNA by quantitative 
RT-PCR, which showed that GnRH induced a rapid, transient increase in Fanca 
mRNA. Fanca protein was also acutely upregulated after GnRH treatment of L beta 
T2 cells. In addition, Fanca gene expression was confined to mature pituitary 
gonadotrophs and adult mouse pituitary and was not expressed in the immature 
alpha T3-1 gonadotroph cell line. Thus, this study extends the expression 
profile of Fanca into a highly specialized endocrine cell and demonstrates 
hormonal regulation of expression of the Fanca locus. We suggest that this 
regulatory mechanism may have a crucial role in the GnRH-response mechanism of 
mature gonadotrophs and perhaps the etiology of FA.