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FDanTra1

ABSTRACT: Danionella cerebrum

PROVIDER: PRJEB38564 | ENA |

REPOSITORIES: ENA

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Dataset's files

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			Action	DRS
		Other
	CAIGQI01.dat.gz	Other
	CAIGQI01.fasta.gz	Fasta.gz
	CAIGQI01.master.dat	Other

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Transcription profiling of human fetal cerebellum, heart, cerebrum, and cerebrum derived astrocyte cell line from trisomy 21 and trisomy 13 samples

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Project description:The purpose of this experiment was to further our understanding of gene expression in the central nervous system (thalamus and cerebrum) after exposure to West Nile virus. To that end, three different analyses were performed. The first examined differences in gene expression between horses not vaccinated and exposed to WNV and normal control horses (exposure). The second examined differences in gene expression between horses not vaccinated and exposed to WNV and horses vaccinated and exposed to WNV (survival). And the third examined differences between the nonvaccinated cerebrum and nonvaccinated thalamus of horses exposed to WNV (location). Six conditions- Gene expression in the thalamus and cerebrum of three different groups of horses (Non-vaccinated horses exposed to West Nile virus, Vaccinated horses exposed to West Nile virus, normal horses not exposed to West Nile virus). Biological replicates- 6 normal cerebrums, 6 normal thalamus, 6 vaccinated and exposed cerebrums, 6 vaccinated and exposed thalamus, 6 non-vaccinated and exposed cerebrum, 6 non-vaccinated and exposed thalamus.

2011-08-31 | E-GEOD-30347 | biostudies-arrayexpress

Does Phosphatidylserine (PS) affect gene expression in FD mice?

Project description:Genes associated with transcription regulation and development processes were up-regulated in the cerebrum of PS-treated mice.

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RNA-Seq analysis of wild-type and Hdac3-null E16.5 neurospheres and P0 cerebral cortex

Project description:Histone deacetylase 3 (HDAC3) is a unique epigenetic regulator forming stoichiometric complexes with several other proteins. Patients with mutations in genes encoding these proteins display intellectual disability, implying an important role of HDAC3 in this prevalent disease. Here we report that cerebrum-specific inactivation of the mouse gene causes striking developmental defects in the neocortex, hippocampus and corpus callosum; post-weaning lethality; and abnormal behaviors, including hyperactivity and anxiety. The developmental defects are due to rapid loss of neural stem and progenitor cells (NSPCs), starting at E14.5. Premature neurogenesis and abnormal neuronal migration in the mutant brain alter NSPC homeostasis. Mutant cerebral cortices display augmented DNA damage, apoptosis, and histone hyperacetylation. In agreement with these results, mutant NSPCs are impaired in forming neurospheres in vitro, and treatment of wild-type NSPCs with the HDAC3-specific inhibitor RGFP966 abolishes neurosphere formation. Transcriptomic analyses of neonatal cerebral cortices and cultured neurospheres support that HDAC3 regulates various transcriptional programs through interaction with multiple transcription factors, including NFIB. These findings establish HDAC3 as a major deacetylase critical for perinatal development of the mouse cerebrum and NSPCs, thereby suggesting a direct link of this enzymatic epigenetic regulator to human cerebral and intellectual development. To study the impact of cerebrum specific (Emx1-Cre) deletion of Hdac3 on embryonic neurospheres (cultured in vitro from E16.5 cerebrum) and neocortex from newborn pups (P0).

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