FolR1 gene ablation-induced changes in gene expression in mouse conotrucus tissue and developing heart

Defective function of FolR1 in mice results in inadequate transport, accumulation, or metabolism of folate during cardiovascular morphogenesis. We have observed cardiovascular abnormalities including outflow track defects and aortic arch artery defects in these genetically compromised mice. In order to investigate the mechanisms underlying the failure to complete cardiac development in the transgenic mouse model, we studied gene expression difference between FolR1 knockout embryos and normal embryos during outflow track septation (GD11:12, GSM78976 ... GSM78987), and studied gene expression difference between FolR1 knockout embryos and normal embryos during embryonic heart development(GD9:00 and GD10:00, GSM79024 ... GSM79035). Keywords: gene ablation response Pregnant FolR1 heterozygotic dams were supplemented with s-folinic acid 6.25mg/kg/day p.o. At GD11:12, 3 control embryos and 3 null embryos were harvested from 6 different dams. From these embryos, the conotruncus tissue of developing heart was dissected and RNA extracted. These RNA samples were used for hybridization on commercially available CodeLink UniSet 10K Bioarray. Pregnant FolR1 heterozygotic dams were supplemented with s-folinic acid 6.25mg/kg/day p.o. At GD9:00 and GD10:00, 3 control embryos and 3 null embryos were harvested from 6 different dams for each timepoint. From these embryos, the heart tissue of developing heart was dissected and RNA extracted. These RNA samples were used for hybridization on commercially available CodeLink UniSet 20K Bioarray.