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Gene expression profile of primary cortical neurons from necdin-null mouse embryo

ABSTRACT: Necdin, a pleiotropic protein expressed predominantly in postmitotic neurons of mammals, regulates neuronal development and survival by interacting with various regulatory proteins. To understand a novel function of necdin, we analyzed gene expression profile of primary cortical neurons prepared from necdin-null mice at embryonic day 14.5.

ORGANISM(S): Mus musculus

PROVIDER: GSE63498 | GEO | 2016/03/10

SECONDARY ACCESSION(S): PRJNA268071

REPOSITORIES: GEO

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Gene expression profile of primary cortical neurons from necdin-null mouse embryo

Project description:Necdin, a pleiotropic protein expressed predominantly in postmitotic neurons of mammals, regulates neuronal development and survival by interacting with various regulatory proteins. To understand a novel function of necdin, we analyzed gene expression profile of primary cortical neurons prepared from necdin-null mice at embryonic day 14.5. Wild-type and necdin-null cortical cells were prepared from mice at embryonic day 14.5. These cells were incubated in Neurobasal medium supplemented with B27 and differentiated into neurons for 4 days (>97% MAP2-positive postmitotic neurons). Three mice per genotype were used for analysis.

2016-03-10 | E-GEOD-63498 | biostudies-arrayexpress

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Transcription profiling of preadipocytes of wild type and IRS-1,IRS-2, IRS-3, IRS-4 knock out mice to reveal role of insulin receptor substrates and necdin

Project description:Insulin and IGF-1 promote adipocyte differentiation via complex and overlapping signalling networks. Here we used microarray analysis of brown preadipocytes derived from wild-type and insulin receptor substrate (IRS) knockout (KO) animals, which exhibited progressively impaired differentiation, to define the set of genes that predict adipogenic potential in these cells. 374 genes/ESTs were identified whose expression in preadipocytes correlated with their ultimate ability to differentiate. Many of these genes were related to early adipogenic events, including genes involved in extracellular matrix, cytoskeletal organization, growth arrest, post-mitotic clonal expansion, and inhibitors of adipogenesis, including preadipocyte factor-1 and multiple members of the Wnt-signalling pathway. Reconstitution of IRS-1 KO cells with IRS-1 reversed these changes and restored the ability to differentiate. Several of these genes showed concordant changes in brown adipose tissue in vivo. Necdin was markedly increased in IRS-1 KO cells that could not differentiate, and knockdown of necdin restored brown adipogenesis with down-regulation of Pref-1 and Wnt10a expression. We demonstrated a necdin-E2F4 interaction repressing PPARg transcription. IRS proteins regulated necdin via a CREB dependent pathway, defining a signalling network involved in brown preadipocyte determination.

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Project description:Assembly of transcriptomes encoding unique neuronal identities requires selective accessibility of transcription factors to cis-regulatory sequences in nucleosome-embedded postmitotic chromatin. Yet, the mechanisms controlling postmitotic neuronal chromatin accessibility are poorly understood. Here, we show that unique distal enhancers define the Pet1 neuron lineage that generates serotonin (5-HT) neurons. Heterogeneous single cell chromatin landscapes are established early in postmitotic Pet1 neurons and reveal the putative regulatory programs driving Pet1 neuron subtype identities. Distal enhancer accessibility is highly dynamic as Pet1 neurons mature, suggesting the existence of regulatory factors that reorganize postmitotic neuronal chromatin. We find that Pet1 and Lmx1b control chromatin accessibility to select Pet1-lineage specific enhancers for 5-HT neurotransmission. Additionally, these factors are required to maintain chromatin accessibility during early maturation suggesting that postmitotic neuronal open chromatin is unstable and requires continuous regulatory input. Together our findings reveal postmitotic transcription factors that reorganize accessible chromatin for neuron specialization.

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