Expression data from 9 and 13 weeks old TIFIAD1Cre mice

We have investigated the p53-dependent stress response in medium spiny neurons (MSNs) that degenerate in Huntington’s disease. To induce p53 signaling cascade, we have genetically inactivated by the Cre/loxP system the essential RNA polymerase I (Pol I) transcription factor TIF-IA, leading to stabilization of p53 and induction of p53-dependent apoptosis. In the present study, we selectively ablated the TIF-IA gene in MSNs by crossing TIF-IAflox/flox mice, homozygous for the floxed TIF-IA allele with transgenic mice expressing the Cre recombinase under the control of the D1 dopamine receptor (D1R) promoter. To explore the molecular mechanisms underlying survival and death we profiled global gene expression in 9 and 13 week old control and TIF-IAD1RCre mutant mice (3 mice/each timepoint For each of the four conditions, five GeneChips were used each )