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Microarray Analysis of Embryonic Kidneys Following Inactivation of GATA3

Mutations of GATA‐3 lead to Hypoparathyroidism, Sensioneural Deafness, and Renal Hypoplasia Syndrome (HDR). The mechanism by which GATA‐3 causes developmental abnormalities remains poorly understood because murine knockouts are embryonic lethal. To overcome this limitation we inactivated GATA‐3 using the floxed exon‐4 GATA‐3 mouse and the temporally regulated Cre‐recombinase CreERT2 transgenic mouse. GATA‐3 was inactivated in embryos by administering a single dose of tamoxifen to the pregnant dams at E11.5 and removed at E14.5. Inactivation of GATA‐3 resulted in smaller kidneys with a 35% reduction in terminal ureteric bud tips; cell proliferation and apoptosis were not significantly different. To better understand the role of GATA3 in renal development cDNA microarray analysis was performed; results show that expression of 191 genes was altered by 2‐fold or more in embryonic kidneys expressing the mutant GATA3 compared to control, with an average fold change of 2.24 ± 0.34. Additional analysis shows that the majority of altered genes in the ureteric bud tip (UB) were down regulated (2.7:1), while the majority of genes in the UB trunk and metanephric mesenchyme were up regulated (18:1 and 2.6:1, respectively). This project discusses the altered gene expression pattern and the novel signaling pathways.