Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Exon level gene expression profile of the prefrontal cortex region of Df(16)A+/- mice, a mouse model of 22q11.2 microdeletion syndrome


ABSTRACT: 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 between mutant and wild type animals at exon level. 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. Adult mutant mice and their wild type littermate were selected. Prefrontal cortex tissues were dissected, total RNA were extracted, processed and hybridized on Affymetrix microarrays. We sought to obtain difference of expression profiles between mutant and wild mice at exon level.

ORGANISM(S): Mus musculus

SUBMITTER: Bin XU 

PROVIDER: E-GEOD-45935 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

The pattern of cortical dysfunction in a mouse model of a schizophrenia-related microdeletion.

Fénelon Karine K   Xu Bin B   Lai Cora S CS   Mukai Jun J   Markx Sander S   Stark Kimberly L KL   Hsu Pei-Ken PK   Gan Wen-Biao WB   Fischbach Gerald D GD   MacDermott Amy B AB   Karayiorgou Maria M   Gogos Joseph A JA  

The Journal of neuroscience : the official journal of the Society for Neuroscience 20130901 37


We used a mouse model of the schizophrenia-predisposing 22q11.2 microdeletion to evaluate how this genetic lesion affects cortical neural circuits at the synaptic, cellular, and molecular levels. Guided by cognitive deficits, we demonstrated that mutant mice display robust deficits in high-frequency synaptic transmission and short-term plasticity (synaptic depression and potentiation), as well as alterations in long-term plasticity and dendritic spine stability. Apart from previously reported re  ...[more]

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