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

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 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE29767 | GEO | 2013/01/17

SECONDARY ACCESSION(S): PRJNA141035

REPOSITORIES: GEO

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

Project description: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. 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.

2013-01-17 | E-GEOD-29767 | biostudies-arrayexpress

Gene profile data from Df(16)A/+ and wild type littermates

Project description:This represents an unbiased evaluation of the transcriptional response in the prefrontal cortex and hippocampus areas in the Df(16)A/+ mice, a mouse model of human 22q11 microdeletion syndrome. 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 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. Keywords: disease state analysis, genetic modification

2008-04-10 | GSE10784 | GEO

Transcription profiling of mouse Df(16)A/+ and wild type littermates

Project description:This represents an unbiased evaluation of the transcriptional response in the prefrontal cortex and hippocampus areas in the Df(16)A/+ mice, a mouse model of human 22q11 microdeletion syndrome. 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 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. Experiment Overall Design: A total of 20 PFC and 20 HPC from 10 Df(16)A/+ mutants and 10 WT control mice was used for RNA extraction and hybridization on Affymetrix microarrays. All mice were male littermates 8 weeks of age.

2008-06-11 | E-GEOD-10784 | biostudies-arrayexpress

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

Project description: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.

2013-10-21 | E-GEOD-45935 | biostudies-arrayexpress

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

Project description: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.

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Mouse models of 17q21.31 microdeletion and microduplication syndromes highlight the importance of Kansl1 for cognition.

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