Fmn2 is almost exclusively expressed in the nervous system [70] and is a strong candidate for a trans-effect specific to neural tissues. However, its precise function in the brain has not been established. Fmn2-null mice do not have notable CNS abnormalities [71], but to evaluate a possible role of Fmn2 on expression of genes that map to Qrr1d, we generated array data from brains of Fmn2-null (Fmn2−/−) and coisogenic (Fmn2+/+) 129/SvEv controls. At a stringent statistical threshold (Bonferroni corrected p<0.05), only eight genes have significant expression differences between Fmn2−/− and Fmn2+/+ genotypes (table 6). Five out of the eight genes, including Pou6f1, Usp53, and Slc11a, have trans-QTLs in Qrr1d. Deletion of Fmn2 had the most drastic effect on the expression of the transcription factor gene Pou6f1, a gene implicated in CNS development and regulation of brain-specific gene expression [72],[73]. Expression of Pou6f1 maps as a trans-QTL (at LOD score of 3) to Qrr1d in the hippocampus dataset, and its expression was down-regulated more than 44-fold in the Fmn2−/− line. While the expression analysis of Fmn2-null mice does not definitively link
