Domestication_gene_expression
Ontology highlight
ABSTRACT:
ORGANISM(S): Oryctolagus cuniculus
SUBMITTER: Frank Albert
PROVIDER: E-MTAB-1249 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:While multiple studies have reported the accelerated evolution of brain gene expression in the human lineage, the mechanisms underlying such change remain poorly understood. Here we address this issue from a developmental perspective, by analyzing mRNA and microRNA (miRNA) expression in two brain regions within macaques, chimpanzees and humans throughout their lifespan. We find that developmental profiles of trans-regulators, such as miRNA, as well as their target genes, show the fastest rates of human-specific evolutionary change. Changes in expression of a few key regulators may be a major driving force behind human brain evolution. Human, chimpanzee and rhesus macaque post-mortem brain samples from the prefrontal cortex and cerebellar cortex were collected. The age ranges of the individuals in all three species covered the respective species' postnatal maturation period from infancy to old adulthood. RNA extracted from the dissected tissue was hybridized to B72.
2011-12-09 | E-GEOD-29356 | biostudies-arrayexpress
Project description:Proteomics offers vast potential to study the molecular regulation of the human brain. Formalin fixation is a common method for preserving human tissue, however, presents challenges for proteomic analysis. In this study we compared the efficiency of two different protein extraction buffers on three post-mortem, formalin-fixed human brains. Equal amounts of extracted proteins were subjected to in-gel tryptic digestion and liquid chromatography-tandem mass spectrometry (LC-MS/MS). Protein, peptide sequence and peptide group identifications, protein abundance and gene ontology pathways were analyzed. Protein extraction was superior using lysis buffer containing Tris (hydroxymethyl) aminomethane hydrochloride, sodium dodecyl sulfate, sodium deoxycholate, and Triton X-100 (TrisHCl, SDS, SDC, Triton X-100), which was then used for inter-regional analysis. Pre-frontal, motor, temporal, and occipital cortex tissue was analyzed by label free quantification (LFQ) proteomics, Ingenuity Pathway Analysis and PANTHERdb. Inter-regional analysis of the human brain revealed differential enrichment of proteins. We found similarly activated cellular signaling pathways, suggesting commonalities in the molecular regulation of neuroanatomically-linked brain functions. Overall, we developed an optimized, robust, and efficient method for protein extraction from formalin-fixed, human brain tissue for in-depth LFQ proteomics. We further demonstrate that this method is suitable for quick analysis of molecular signaling pathways in the human brain.
2023-02-22 | PXD039808 | Pride
Project description:Cerebellar cortex expression in ataxia-telangiectasia patients and normal controls. The neurodegenerative disease known as ataxia-telangiectasia (A-T) is caused by the absence of the ATM (A-T mutated) protein. A long-standing mystery surrounding A-T is why cerebellar Purkinje cells (PCs) appear uniquely vulnerable to ATM-deficiency. Here, we present that 5-hydroxymethylcytosine (5hmC), a newly recognized epigenetic marker found at high levels in neurons, is substantially reduced in human A-T and Atm-/- mouse cerebellar PCs. TET1, an enzyme that converts 5mC to 5hmC, responds to DNA damage. Manipulation of TET1 activity directly affects neuronal cell cycle reentry and cell death after the induction of DNA damage. Quantitative, genome-wide analysis of 5hmC of samples from human cerebellum showed that in ATM-deficiency there is a remarkable genome-wide reduction of 5hmC enrichment at both proximal and distal regulatory elements. These results reveal a role of TET1-mediated 5hmC in DNA damage response, and provide insights into the basis of a PC-specific DNA demethylation alteration in ATM-deficiency. Human frozen tissue was obtained from the NICHD Brain and Tissue Bank of Developmental Disorders at the University of Maryland, Baltimore, MD. RNA was prepared and run on an Illumina Human HT-12 v4 microarray. 3 ataxia-telangiectasia (A-T) cases and 4 normal controls.
2015-10-30 | E-GEOD-61019 | biostudies-arrayexpress
Project description:RNA extracted from human frontal cortex area 8, the main area afected in FTLD, of controls (n=10), sporadic FTLD-TDP (sFTLD) (n=10) and C9ORF72-familial FTLD (fFTLD) (n=10) samples were analyzed using the Affymetrix Clariom™ D Assay, human (Affymetrix ref.902923). The present study identifies the main gene deregulation between sporadic forms of FTLD-TDP (sFTLD) and the major and most common genetic cause of FTLD, the C9ORF72 repeat expansion (fFTLD), when compare with control samples.
2018-09-19 | E-MTAB-6189 | biostudies-arrayexpress
Project description:Proteomic sequencing of postmortem human brain can identify dysfunctional proteins that contribute to neurodegenerative disorders like Alzheimer’s disease and frontotemporal dementia. Similar studies in chronic traumatic encephalopathy are limited, but may provide important new insights into this disorder. Given our previous success with identifying pathology associated proteins, we performed proteomic sequencing of detergent insoluble brain homogenates from frontal cortex of deceased subjects with CTE covering a range of CTE pathologic stages. We compared the insoluble proteome of CTE brain to control and AD brains to identify differentially expressed proteins. We identified over 4000 proteins in CTE brains, including significant enrichment of the microtubule associated protein tau. We also found enrichment and pathologic aggregation of RNA processing factors as seen previously in AD, supporting the previously recognized overlap between AD and CTE. In addition to these similarities, we identified CTE-specific enrichment of a number of proteins which increase with increasing severity of CTE pathology. NADPH dehydrogenase quinone 1 (NQO1) was one of the proteins which showed significant enrichment in CTE and also correlated with increasing CTE stage. NQO1 demonstrated neuropathologic correlation with hyperphosphorylated tau in glial cells, mainly astrocytes. These results demonstrate that quantitative proteomic sequencing of CTE postmortem human brain can identify disease relevant findings and novel cellular pathways involved in CTE pathogenesis.
2017-11-27 | PXD007694 | Pride
Project description:We have quantified gene expression in five tissues (brain, heart, kidney, liver and testis) from humans, chimpanzees and rhesus macaques using the Illumina NlaIII Digital Gene Expression (DGE) protocol. This dataset extends a previous microarray study by Khaitovich et al. (Khaitovich et al. 2005) with the rhesus macaque outgroup and complements other previously generated tissue transcriptome profiles from primates (Enard et al. 2002; Khaitovich et al. 2006; Somel et al. 2009; Babbitt et al. 2010; Blekhman et al. 2010; Wetterbom et al. 2010). contributor: Max Planck Institute for Evolutionary Anthropology, Deutscher Platz 6, D-04103 Leipzig, Germany Samples were obtained from brain (pre-frontal cortex), heart, kidney, liver, and testis tissues of male humans, chimpanzees and rhesus macaques. Illumina NlaIII DGE libraries for all samples were generated in tissue batches, randomizing species in library preparation and sequencing. Human samples originate from different, probably unrelated, individuals for each tissue. For chimpanzees and rhesus macaques the libraries for all tissues come from the same set of individuals and among these are individuals related at the half- and full-sibling level. Due to limited access to samples, the analysis could not be limited to individuals of similar age. Human individuals vary between 5 and 88 years of age, chimpanzees between 6 years and 35 years of age and rhesus macaques between 3 and 9 years of age.
2013-10-01 | E-GEOD-50782 | biostudies-arrayexpress
Project description:There is accumulating evidence that amyloid beta and tau proteins may act synergistically to cause synapse and neural circuit degeneration in Alzheimer’s disease. In order to study this, we designed a new mouse model which lacks endogenous mouse tau, but expresses both the APP/PS1 transgene, which causes well-characterised plaque-associated synapse loss, and also reversibly expresses wild-type human tau (which can be suppressed with doxycycline). We examined the transcriptional changes in the frontal cortex of this mouse model, along with behaviour, pathology, synaptic plasticity, synapse degeneration and accumulation of amyloid beta and tau at synapses, and compared with littermate control genotypes: those lacking endogenous mouse tau, those lacking endogenous mouse tau but expressing the APP/PS1 transgene only, and those lacking endogenous mouse tau but reversibly expressing wild-type human tau only.
2019-11-12 | E-MTAB-7856 | biostudies-arrayexpress
Project description:The inbred LOU/C/Jall rat is currently described as a model of successful aging. These rats have a longer healthy median lifespan than other strains, do not develop obesity, diabetes, or tumor and more importantly they do not show cognitive decline with aging. This is the first study to examine gene expression changes in the inbred LOU/C/Jall rat hippocampus and frontal cortex. Microarray data from LOU/C/Jall rats aged of 5 months were compared to the one measured in rats aged of 26 month. We have identified a set of 15 genes in the hippocampus and 70 genes in the frontal cortex that could be grouped into several clusters of similar expression profiles and that are involved in biological functions, namely regulation of plasticity, inflammatory response, metabolic, catabolic and homeostatic processes, and transcription. Genes were mainly up-regulated in aged brain. Gene expression profil in hippocampus and cortex frontal of LOU/C/Jall rats strain. Rats were 3 and 26 months old.
2012-10-01 | E-GEOD-36722 | biostudies-arrayexpress
Project description:To identify molecular pathological alterations in AD brains, we performed interspecies comparative microarray analyses using RNAs prepared from postmortem human brain tissues donated for the Hisayama study and hippocampal RNAs from the triple-transgenic mouse model of AD (3xTg-AD) Three-way ANOVA of microarray data from frontal cortex, temporal cortex and hippocampus with presence/absence of AD and vascular dementia, and sex, as factors revealed that the gene expression profile is most significantly altered in the hippocampi of AD brains. Comparative analyses of the brains of AD patients and a mouse model of AD showed that genes involved in non-insulin dependent DM and obesity were significantly altered in both, as were genes related to psychiatric disorders and Alzheimer’s disease. We prepared RNA samples from the gray matter of frontal and temporal cortices and hippocampi derived from 88 postmortem brains, among which 26 cases were pathologically diagnosed as having AD or an AD-like disorder. High-quality RNA (RIN≧6.9) samples were subjected to microarray analysis using the Affymetrix Human Gene 1.0 ST platform, and only those results that passed examinations for quality assurance and quality control of the Human Gene 1.0 ST arrays were retrieved. In total, we obtained gene expression profiles from the following samples: 33 frontal cortex samples, among which 15 were from AD patients; 29 temporal cortex samples, among which 10 were from AD patients; 17 hippocampus samples, among which seven were from AD patients
2013-04-17 | E-GEOD-36980 | biostudies-arrayexpress
Project description:The goal of the study was to compare gene expression of P0 wild-type and P0 Satb2-/- cortices. Total RNAs were isolated from P0 cortices dissected from wild-type and Satb2-/- mice (n=3 for each genotype), following Qiagen RNAeasy kit instruction.Sequence libraries were made following Illumina RNA TruSeq library preparation guide.The libaries were pair-end sequenced (50nt per end). Differentially expressed genes were identified by DESEQ. Total RNAs were isolated from P0 cortices (3 control and 3 mutants), and sequenced on Illumina Genome Analyzer
2015-09-08 | E-GEOD-68911 | biostudies-arrayexpress