Neuro-specific HuR-deficient mice spontaneously develop motor neuron disease

To study the neuron-specific function of HuR, we generated inducible, neuron-specific HuR-deficient mice of both sexes. These mice developed a phenotype consisting of poor balance, decreased movement, and decreased strength Genome-wide microarray and RT-PCR analysis further indicated that HuR deficiency in neurons resulted in altered expression of genes in the brain involved in cell growth The additional enriched GO terms in the brain tissues of neuron-specific HuR-deficient mice were largely related to inflammation, including interferon-induced genes and complement components. We generated conditional neuron-specific HuR-deficient mice (Thy1Cre-ERT2-EYFPHuRf/f, designed as KO) and control mice (Thy1Cre-ERT2-EYFPHuRf/+, designed as wild type, WT). Cre expression was induced through Tamoxifen administration to conditional neuron-specific HuR-deficient mice (Thy1Cre-ERT2-EYFPHuRf/f) and control mice (Thy1Cre-ERT2-EYFPHuRf/+) of either sex at 10 and 11 weeks of age (Fig. 1A). Cre-YFP expression was highly induced 21 days after first tamoxifen administration. Then RNA was extractedfrom total brain tissues from neuron-specific HuR-deficient and control mice to perform Mouse Gene 2.0 ST microarray.