Gene expression profiles in the hippocampi and prefrontal cortex of Df16(A)+/- mice at embryonic day 17, postnatal day 6, and adult stages. Mus musculus

Df16(A)+/- mice line is a model of human 22q11 microdeletion syndrome. We conducted an unbiased evaluation of the transcriptional difference in the prefrontal cortex and hippocampus areas between mutant and wild type animals at two early developmental stages (embryonic day 17 and postnatal day 6). These mice were generated by chromosomal engineering and carry a microdeltion of ~1.3Mb in the mouse locus syntenic to the human 22q11.1 The reasoning behind this expression profiling is that consistent alterations in transcriptional programs reflect either downstream (immediate or remote) effects of the deficiency or reactive (compensatory) changes, and can thus point to affected biological processes and molecular functions. Df(16)A+/- mice line is a model of human 22q11 microdeletion syndrome and Dp(16)B mice line is a model of human 22q11 microduplication. We conducted an unbiased evaluation of the transcriptional difference in the prefrontal cortex and hippocampus areas between the mice with microdeletion, microduplication and heterogygous balanced normal copy number of the mouse syntenic locus. Overall design: Mutant mice and their wild type littermate from two development stages (embryonic day 17 and postnatal day 6) were selected. Hipocampal and prefrontal cortex tissues were dissected, total RNA were extracted, processed and hybridized on Affymetrix microarrays. We sought to obtain temporal gene expression difference of expression profiles between mutant and wild mice. Adult male mice of microdeletion, microduplication were used and mice with heterozygous balanced copy number as reference. Hipocampal and prefrontal cortex tissues were dissected, total RNA were extracted, processed and hybridized on Affymetrix microarrays. we attempted to distinguish primary versus secondary gene targets of the 22q11.2 microdeletion by looking for genes whose expression changes in negative correlation as a result of genomic losses or gains in this locus.