Unknown,Transcriptomics,Genomics,Proteomics

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Gene expression profiling of NCAM-deficient mouse brain

ABSTRACT: Analysis of brains of mice lacking the neural cell adhesion molecule NCAM (Ncam-/-) in comparison to wild-type mice of same age and genetic background (Ncam+/+). NCAM-deficient mice exhibit deficits in long-term potentiation and spatial learning, as well as increased intermale aggression. We performed a microarray analysis of adult NCAM-deficient mouse brains to identify molecular targets which might underly the phenotype of NCAM-deficient mice. We analyzed the gene expression profiles in 2-3 months old (young adult) mouse brains, with both the Ncam-/- and the Ncam+/+ group consisting of three individuals each. Wild-type and NCAM-deficient animals had the same genetic background. RNA was prepared from total brain.

ORGANISM(S): Mus musculus

SUBMITTER: Thomas Streichert

PROVIDER: E-GEOD-16647 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Short DNA sequences inserted for gene targeting can accidentally interfere with off-target gene expression.

Meier Ingo D ID Bernreuther Christian C Tilling Thomas T Neidhardt John J Wong Yong Wee YW Schulze Christian C Streichert Thomas T Schachner Melitta M

FASEB journal : official publication of the Federation of American Societies for Experimental Biology 20100128 6

Targeting of genes in mice, a key approach to study development and disease, often leaves a neo cassette, loxP, or FRT sites inserted in the mouse genome. Insertion of neo can influence the expression of neighboring genes, but similar effects have not been reported for loxP sites. We therefore performed microarray analyses of mice in which the Ncam or the Tnr gene were targeted either by insertion of neo or loxP/FRT sites. In the case of Ncam, neo, but not loxP/FRT insertion, led to a 2-fold red ...[more]

PMID: 20110269

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Project description:Animal and human studies suggest that inflammation is associated with behavioral disorders including aggression. We have recently shown that physical aggression of boys during childhood is strongly associated with reduced plasma levels of cytokines IL-1a, IL-4, IL-6, IL-8 and IL-10, later in early adulthood (Provencal et al., unpublished data). This study tests the hypothesis that there is an association between differential DNA methylation regions in cytokine genes in T cells and monocytes DNA in adult subjects and a trajectory of physical aggression from childhood to adolescence. We compared the methylation profiles of the entire genomic loci encompassing the IL-1a, IL-6, IL-4, IL10 and IL8 and three of their regulatory transcription factors (TF) NFkB1, NFAT5 and STAT6 genes in adult males on a chronic physical aggression trajectory (CPA) and males with the same background who followed a normal physical aggression trajectory (control group). We used the method of methylated DNA immunoprecipitation (MeDIP) with comprehensive cytokine gene loci and TF loci microarray hybridization, statistical analysis and false discovery rate correction. We recruited two groups of Caucasian males who were born in families with a low socioeconomic status and were living at the time of the present study within 200km from our laboratory. The first group, composed of 8 subjects, had a history of chronic physical aggression from age 6 to 15 years (chronic physical aggression group, CPA). The second group, composed of 12 subjects, was recruited from the same longitudinal studies but included only those who did not have a history of chronic physical aggression from age 6 to 15 (Control group, CG). Using custom-designed microarrays with 44K probes tiling cytokines IL-1a, IL-6, IL-4, IL10 and IL8 and three of their regulatory transcription factors (TF) NFkB1, NFAT5 and STAT6, we obtained DNA methylation profiles by meDIP-chip. Each profile was generated in triplicate.

Dataset Information

Gene expression profiling of NCAM-deficient mouse brain

Publications

Short DNA sequences inserted for gene targeting can accidentally interfere with off-target gene expression.

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