Project description:Four sets of six microarray experiments were conducted. Six individual RTT frontal cortices were co-hybridized with six individual control frontal cortices. For example, the frontal cortex of patient RTT1 was compared with the occipital cortex of RTT1. Additionally, where the frontal cortex of a RTT sample was compared to the frontal cortex of a control sample, the comparison between the occipital cortices was conducted between the same samples. For example RTT1 frontal cortex vs. Con4 frontal cortex, RTT1 occipital cortex vs. Con4 occipital cortex. Each experiment was repeated and the fluorescent cyanine dyes were reversed.
Project description:We demonstrate using conditional mutagenesis that Pbx1, with and without Pbx2+/ sensitization, regulates regional identity and laminar patterning of the developing mouse neocortex in cortical progenitors (Emx1-Cre) and in newly generated neurons (Nex1-Cre). Pbx1/2 mutants have three salient molecular phenotypes of cortical regional and laminar organization: hypoplasia of the frontal cortex, ventral expansion of the dorsomedial cortex, and ventral expansion of Reelin expression in the cortical plate of the frontal cortex, concomitant with an inversion of cortical layering in the rostral cortex. Molecular analyses, including PBX ChIP-seq, provide evidence that PBX promotes frontal cortex identity by repressing genes that promote dorsocaudal fate. Chromatin immunoprecipitation was performed using antibody against Pbx1/2/3/ (sc-888, Santa Cruz). Wild type E12.5 mouse whole cortex was used for the analysis.
Project description:We demonstrate using conditional mutagenesis that Pbx1, with and without Pbx2+/ sensitization, regulates regional identity and laminar patterning of the developing mouse neocortex in cortical progenitors (Emx1-Cre) and in newly generated neurons (Nex1-Cre). Pbx1/2 mutants have three salient molecular phenotypes of cortical regional and laminar organization: hypoplasia of the frontal cortex, ventral expansion of the dorsomedial cortex, and ventral expansion of Reelin expression in the cortical plate of the frontal cortex, concomitant with an inversion of cortical layering in the rostral cortex. Molecular analyses, including PBX ChIP-seq, provide evidence that PBX promotes frontal cortex identity by repressing genes that promote dorsocaudal fate. Chromatin immunoprecipitation was performed using antibody against Pbx1/2/3 (sc-888, Santa Cruz). Wild type E15.5 mouse whole cortex was used for the analysis.
Project description:In this study, we investigated the effects of prenatal bisphenol-A (BPA) exposure on transcriptome profiles in the frontal cortex of the rat offspring. Transcriptome profiling by RNA-seq analysis of frontal cortex tissues isolated from neonatal pups prenatally exposed to BPA revealed that a list of differentially expressed genes (DEGs) associated with autism spectrum disorder (ASD), including Ntng1, Auts2, and Ankrd11 was dysregulated in a sex-specific pattern. The gene ontology analysis revealed that the BPA-responsive genes in the offspring’s frontal cortex were significantly associated with ASD-related neurological functions. These results indicated that prenatal BPA exposure may increase the risk of ASD by impacting ASD-related genes in the offspring’s frontal cortex. We conducted experiments using the frontal cortex from neonatal pups prenatally exposed to BPA or vehicle control (BPA treament; pooled 3 pups frontal cortex, vehicle control; pooled 3 pups frontal cortex). 10-week-old female rats were daily treated with BPA at the concentration of 5,000 microgram/kilogram of maternal body weight or vehicle control from gestation day 1 (GD1) until parturition. Total RNAs were isolated and cDNAs were synthesized. The transcriptome profiles were performed using a high-throughtput RNA-seq.
Project description:Here we used mass spectrometry-based proteomics technology to explore SEPs with potential function in five brain regions of the mouse. SEPs with unique peptides were identified in hippocampus, frontal cortex, temporal cortex, occipital cortex and parietal cortex.
Project description:<p>This study utilized neurologically normal control samples deposited in North American Brain Expression Consortium (NABEC). This top-level study, phs001300, makes available all phenotype data of the NABEC study participants. <br/>In addition, molecular data of six sub-studies are available through dbGaP: <ol> <li>NABEC Genome-Wide Genotyping - <a href="study.cgi?study_id=phs000249">phs000249</a></li> <li>NABEC Exome Sequencing - <a href="study.cgi?study_id=phs001301">phs001301</a></li> <li>NABEC CAGE Sequencing of Human Cerebral Frontal Cortex - <a href="study.cgi?study_id=phs001302">phs001302</a></li> <li>NABEC mRNA Sequencing of human Cerebral Frontal Cortex - <a href="study.cgi?study_id=phs001353">phs001353</a></li> <li>NABEC Total RNA Sequencing of human Cerebral Frontal Cortex - <a href="study.cgi?study_id=phs001354">phs001354</a></li> <li>NABEC Neurochip Genotyping - <a href="study.cgi?study_id=phs001462">phs001462</a></li> </ol> </p>
Project description:We used single-cell whole genome sequencing (scWGS) to assess aneuploidy in isolated neurons from the frontal cortex of control individuals. This experiment is related to E-MTAB-4184, which contains Alzheimer's disease samples.