Version: 8.0.0Date: Tue Jan 28 2025
Category
CFP
(Homo sapiens)Gene
Name: complement factor properdin
Synonyms: BFD, properdin, complement factor P, PFC, PFD, properdin P factor, complement
Source: HGNC:8864
Biotype: protein coding gene
Synonyms: PFC...PFC
Cfp
(Mus musculus)Gene
Name: complement factor properdin
Synonyms: properdin factor, complement, Pfc
Source: MGI:97545
Biotype: protein coding gene
Synonyms: Pfc...Pfc
cfp.L
(Xenopus laevis)Gene
Name: complement factor properdin
Synonyms: bfd, properdin, cfp.L, complement factor properdin, pfc
Source: Xenbase:XB-GENE-5941338
Biotype: gene
Synonyms: pfc...pfc...pfc
Cfp
(Rattus norvegicus)Gene
Name: complement factor properdin
Synonyms: properdin factor, complement (mapped), Pfc_mapped, properdin, Properdin P factor, complement, properdin factor, complement, Pfc
Source: RGD:1594557
Biotype: protein coding gene
Synonyms: Pfc...Pfc
rat PFC: Sham vs. SNI
(Rattus norvegicus)HTP Dataset Index
High-Throughput (HTP) Dataset Index metadata provided by RGD
ID: GEO:GSE70006
Tags: unclassified
Summary: DNA methylation profiles of prefrontal cortec (PFC) comparing 9 months post Spared Nerve Injury (SNI) rats with Sham rats.
Symbol: rat PFC: Sham vs. SNI
Olanzapine vs. Saline rat pfc
(Rattus norvegicus)HTP Dataset Index
High-Throughput (HTP) Dataset Index metadata provided by RGD
ID: GEO:GSE2547
Tags: unclassified
Summary: Keywords: repeat sample
Symbol: Saline rat pfc
Name: Saline rat pfc
Male Rat DNA methylation in the Prefrontal Cortex at postnatal day 62 following prenatal restraint stress
(Rattus norvegicus)HTP Dataset Index
High-Throughput (HTP) Dataset Index metadata provided by RGD
ID: GEO:GSE84021
Tags: unclassified
Summary: DNA methylation profiling of Prefrontal Cortex of male rats at postnatal day 62 whose mothers were exposed to restraint stress from gestation day 14 until delivery
Cell/ Tissues: PFC
Transcriptional profiling of Rat PFC 2 hours after the beginnig of stress
(Rattus norvegicus)HTP Dataset Index
High-Throughput (HTP) Dataset Index metadata provided by RGD
ID: GEO:GSE224313
Tags: unclassified
Summary: Samples were collected from rats exposed to FS stress and sacrificed 2 hours after the beginnig of 40-minutes stress section and from controls left undisturbed in their cage
Symbol: Transcriptional profiling of Rat PFC 2 hours after the beginnig of stress
Name: Transcriptional profiling of Rat PFC 2 hours after the beginnig of stress
Transcriptional profiling of Rat PFC after footshock stress
(Rattus norvegicus)HTP Dataset Index
High-Throughput (HTP) Dataset Index metadata provided by RGD
ID: GEO:GSE224312
Tags: unclassified
Summary: Samples were collected from rats exposed to FS stress and sacrificed immediately after the 40-minutes stress section and from controls left undisturbed in their cage
Symbol: Transcriptional profiling of Rat PFC after footshock stress
Name: Transcriptional profiling of Rat PFC after footshock stress
Cfpem1Gpt
(Mus musculus)Allele/Variant
Source: MGI:7296888
Genes: Cfp (Mmu)
Synonyms: Not Available
Variant Type: unreported
Molecular Consequence: Not Available
Diseases: Not Available
Variant Name: Not Available
Gene Synonyms: Pfc
Cfptm1.1Song
(Mus musculus)Allele/Variant
Source: MGI:3771611
Genes: Cfp (Mmu)
Synonyms: Not Available
Variant Type: unreported
Molecular Consequence: Not Available
Diseases: Not Available
Variant Name: Not Available
Gene Synonyms: Pfc
Cfpem1Smoc
(Mus musculus)Allele/Variant
Source: MGI:7288948
Genes: Cfp (Mmu)
Synonyms: Not Available
Variant Type: unreported
Molecular Consequence: Not Available
Diseases: Not Available
Variant Name: Not Available
Gene Synonyms: Pfc
Cfptm1Song
(Mus musculus)Allele/Variant
Source: MGI:3771610
Genes: Cfp (Mmu)
Synonyms: Not Available
Variant Type: unreported
Molecular Consequence: Not Available
Diseases: Not Available
Variant Name: Not Available
Gene Synonyms: Pfc
Cfptm2.1Song
(Mus musculus)Allele/Variant
Source: MGI:4838300
Genes: Cfp (Mmu)
Synonyms: Not Available
Variant Type: unreported
Molecular Consequence: Not Available
Diseases: Not Available
Variant Name: Not Available
Gene Synonyms: Pfc
Cfptm1Cmst
(Mus musculus)Allele/Variant
Source: MGI:3774548
Genes: Cfp (Mmu)
Synonyms: Not Available
Variant Type: unreported
Molecular Consequence: Not Available
Diseases: Not Available
Variant Name: Not Available
Gene Synonyms: Pfc
Cfpem1(IMPC)H
(Mus musculus)Allele/Variant
Source: MGI:7425583
Genes: Cfp (Mmu)
Synonyms: Not Available
Variant Type: unreported
Molecular Consequence: Not Available
Diseases: Not Available
Variant Name: Not Available
Gene Synonyms: Pfc
RNA editing in the Rat brain
(Rattus norvegicus)HTP Dataset Index
High-Throughput (HTP) Dataset Index metadata provided by RGD
ID: GEO:GSE99214
Tags: unclassified
Summary: Adenosine-to-inosine (A-to-I) RNA editing is an epigenetic modification catalyzed by adenosine deaminases acting on RNA (ADARs), and is especially prevalent in the brain.Using microfluidics-based multiplex PCR sequencing (mmPCR-seq) to assess A-to-I editing at 146 pre-selected, conserved sites, we found that editing was generally higher in adult compared to neonatal rat brain, and that at birth, global editing was lower in prefrontal cortex than in amygdala. Prereproductive stress (PRS) affected editing at the serotonin receptor 2c, and editing at this site was significantly altered in offspring of PRS rats across two generations. Changes in ADAR expression did not correlate with editing changes induced by development or stress. Our findings indicate that mmPCR-seq can accurately detect RNA editing in rat brain samples, and confirm previous accounts of a developmental increase in RNA editing rates. Altered RNA editing rates in offspring of stress-exposed rats complements growing literature on the transgenerational effects of stress.
Cell/ Tissues: PFC
Cannabinoid exposure in adolescence reprograms the PFC’s molecular response to cocaine
(Rattus norvegicus)HTP Dataset Index
High-Throughput (HTP) Dataset Index metadata provided by RGD
ID: GEO:GSE134935
Tags: unclassified
Summary: There are still no neurobiological data on whether prior cannabinoid exposure modifies the brain’s molecular response to cocaine. We investigated epigenomics, transcriptomics to characterize molecular changes in subcellular PFC compartments, including nucleus, cytoplasm and synaptosomes.
Cell/ Tissues: PFC
Name: Cannabinoid exposure in adolescence reprograms the PFC’s molecular response to cocaine
Symbol: Cannabinoid exposure in adolescence reprograms the PFC’s molecular response to cocaine
Transcriptional profiling of Rat PFC 24 hours after the beginnig of stress
(Rattus norvegicus)HTP Dataset Index
High-Throughput (HTP) Dataset Index metadata provided by RGD
ID: GEO:GSE224314
Tags: unclassified
Summary: Samples were collected from rats exposed to FS stress and sacrificed 24 hours after the beginnig of 40-minutes stress section and from controls left undisturbed in their cage
Symbol: Transcriptional profiling of Rat PFC 24 hours after the beginnig of stress
Name: Transcriptional profiling of Rat PFC 24 hours after the beginnig of stress
HTP Dataset Index
High-Throughput (HTP) Dataset Index metadata provided by RGD
ID: GEO:GSE246666
Tags: unclassified
Summary: Social behavioral changes are a hallmark of several neurodevelopmental and neuropsychiatric conditions, nevertheless the underlying neural substrates of such dysfunction remain poorly understood. Building evidence points to the prefrontal cortex (PFC) as one of the key brain regions that orchestrates social behavior. We used this concept with the aim to develop a translational rat model of social-circuit dysfunction, the chronic PFC activation model (CPA). Chemogenetic designer receptor hM3Dq was used to induce chronic activation of the PFC over 10 days, and the behavioral and electrophysiological signatures of prolonged PFC hyperactivity were evaluated. To test the sensitivity of this model to pharmacological interventions on longer timescales, and validate its translational potential, the rats were treated with our novel highly selective oxytocin receptor (OXTR) agonist RO6958375, which is not activating the related vasopressin V1a receptor. CPA rats showed reduced sociability in the three-chamber sociability test, and a concomitant decrease in neuronal excitability and synaptic transmission within the PFC as measured by electrophysiological recordings in acute slice preparation. Sub-chronic treatment with a low dose of the novel OXTR agonist following CPA interferes with the emergence of PFC circuit dysfunction, abnormal social behavior and specific transcriptomic changes. These results demonstrate that sustained PFC hyperactivity modifies circuit characteristics and social behaviors in ways that can be modulated by selective OXTR activation and that this model may be used to understand the circuit recruitment of prosocial therapies in drug discovery.
HTP Dataset Index
High-Throughput (HTP) Dataset Index metadata provided by MGI
ID: ArrayExpress:GSE61529
Tags: anatomical structure, baseline
Summary: Time dependent coordinated hippocampal-prefrontal cortical interactions are required for the long-term storage of memories. However, the role of prefrontal cortex (PFC) in encoding of long-term memories remains elusive. Here, we discover a critical role of PFC in the encoding of contextual memories in mice. We demonstrate that specific pools of mRNAs are translated in the PFC following one and six hours of behavioral training. Moreover, disruption of protein synthesis in the prelimbic region of PFC immediately after training inhibits encoding contextual fear memories, whereas disruption at six hours after training is ineffective. Thus, early protein synthesis in the PFC is necessary and critical for the encoding of contextual fear memories. These findings establish key role for the prelimbic cortex in encoding of contextual memories. Examination of polyribosome associated mRNAs in the prefrontal cortex of 8 adult mice following one hour and six hour after contextual fear conditioning.
Expression data from rat prefrontal cortex administrated with MK-801
(Rattus norvegicus)HTP Dataset Index
High-Throughput (HTP) Dataset Index metadata provided by RGD
ID: GEO:GSE220510
Tags: unclassified
Summary: Schizophrenia is a group of severe mental disorders. MK-801 is a common chemical that is used to construct schizophrenic animal model. In the present study, male SD rats were received MK-801 (0.2 mg/kg) intraperitoneal injections for 2 weeks. PFC tissue samples were collected freshly when sacrificing the rats and then quickly frozen and stored under -80°C for RNA sequencing. Differentially-expressed genes (DEGs) were determined by using DESeq2. A total of 129 DEGs, including 50 down-regulated and 79 up-regulated DEGs, were determined. By comparing with the online database TargetScanHuman (Release 8.0) and miRDB (Version 6.0), we found 4 genes (SIK1, TWIST1, BTG2, EGR2) that were altered in the schizophrenic model rat PFC and also are potential targets of miR-25.
Genetically distinct parallel projection populations from ventral hippocampus to prefrontal cortex
(Mus musculus)HTP Dataset Index
High-Throughput (HTP) Dataset Index metadata provided by MGI
ID: ArrayExpress:GSE225512
Tags: anatomical structure, baseline
Summary: To investigate differential RNA expression in two populations of ventral CA1 neurons that project to PFC arising from the superficial and deep layers of the radial axis Comparative gene expression profiling analysis of RNA-seq data for superficial vs deep vCA1 neurons
DNA Methyltransferase 3A Mediates the Sustained Effects of Stress on Synaptic Functions and Behaviors [RNA-seq]
(Rattus norvegicus)HTP Dataset Index
High-Throughput (HTP) Dataset Index metadata provided by RGD
ID: GEO:GSE147845
Tags: unclassified
Summary: Emerging evidence suggests that epigenetic mechanisms regulate aberrant gene transcription in stress-associated mental disorders. However, it remains to be elucidated about the role of DNA methylation and its catalyzing enzymes, DNA methyltransferases (DNMTs), in this process. Here we found that rats exposed to chronic (2-week) unpredictable stress exhibited a substantial reduction of Dnmt3a after stress cessation in the prefrontal cortex (PFC), a key target region of stress. Treatment of unstressed control rats with DNMT inhibitors recapitulated the effect of chronic unpredictable stress on decreased AMPAR expression and function in PFC. In contrast, overexpression of Dnmt3a in PFC of stressed animals prevented the loss of glutamatergic responses. Moreover, the stress-induced behavioral abnormalities, including the impaired recognition memory and aggressive behaviors, were ameliorated by Dnmt3a expression in PFC of stressed animals. Lastly, we found genome-wide DNA methylation changes in PFC of stressed rats are selectively enriched at several pathways, such as axon guidance, Wnt signaling and neurotransmission. These findings have therefore recognized the role of DNA epigenetic modification in stress-induced disturbance of synaptic functions and cognitive & emotional processes.
Influence of the early stress of maternal separation on the prefrontal cortex transcriptome
(Rattus norvegicus)HTP Dataset Index
High-Throughput (HTP) Dataset Index metadata provided by RGD
ID: GEO:GSE14720
Tags: unclassified
Summary: Exposure to early stress (ES) is known to enhance adult vulnerability for anxiety and depressive behaviors. The molecular and cellular pathways altered in response to ES that contribute to the establishment of a substrate for susceptibility to adult psychopathology are not well understood. Focusing on the prefrontal cortex (PFC), a brain region implicated in the modulation of emotional responses, we examined the consequences of the early stress experience of maternal separation (MS) on the adult PFC transcriptome. Microarray analysis identified alterations in genes associated with signal transduction, neuronal excitability, G-protein signaling and stress responses in the PFC of adult animals previously exposed to ES. Our results also indicated that the pattern of gene expression changes observed in ES animals contains a component in common with that induced by 5-HT2A/C receptor stimulation in control animals, suggesting enhanced 5-HT2A/C receptor-mediated signaling in ES animals. Further, our microarray results reveal that a history of ES alters the DOI-induced transcriptome in the PFC.
Comparison of gene expression profiles in blood, hippocampus and prefrontal cortex in rats
(Rattus norvegicus)HTP Dataset Index
High-Throughput (HTP) Dataset Index metadata provided by RGD
ID: GEO:GSE49352
Tags: unclassified
Summary: This study provides a baseline analysis of absolute gene expression and its differences in blood, PFC and HC brain tissue in genetically identical rats. Our data might be used for first information on gene expression levels of genes of interest in blood and brain under baseline conditions.
Source: DOID:0111768
Definition: A complement deficiency characterized by decreased plasma levels of complement factor properdin and increased susceptibility to Neisseria species infections that has_material_basis_in homozygous or hemizygous mutation in PFC on chromosome Xp11.23.
Brain region-specific changes in neurons and glia and dysregulation of dopamine signaling in Grin2a mutant mice [snRNA-seq]
(Mus musculus)HTP Dataset Index
High-Throughput (HTP) Dataset Index metadata provided by MGI
ID: ArrayExpress:GSE218572
Tags: WT vs. mutant, anatomical structure, age, genotype
Summary: To identify which brain cell types are contributing to the bulk transcriptomic changes in Grin2a mutant mice, we performed single-nucleus RNAseq (snRNAseq) in Grin2a heterozygous and homozygous mutants and their wild-type littermates at 4 and 12 weeks of age. SnRNAseq analysis of prefrontal cortex (PFC), somatosensory cortex (SSC), hippocampus (HP), striatum (ST) and Thalamus (TH) at 12 weeks, as well as PFC and HP at 4 weeks in Grin2a mutant mice.
Cell type-specific mechanism of Setd1a heterozygosity in schizophrenia pathogenesis [bulk RNA-seq]
(Mus musculus)HTP Dataset Index
High-Throughput (HTP) Dataset Index metadata provided by MGI
ID: ArrayExpress:GSE181024
Tags: WT vs. mutant, genotype
Summary: Schizophrenia (SCZ) is a chronic, serious mental disorder with severe burden on patients' families and society. Although over 100 genes have been linked to SCZ pathogenies, the underlying molecular and cellular mechanisms remain largely unknown. Here, we generated a Setd1a haploinsufficiency mouse model to understand how this SCZ-associated epigenetic factor affects gene expression programs in cells of brain regions highly relevant to SCZ. By comparing single-cell RNA-seq results from wild type and Setd1a+/- mice, we found Setd1a heterozygosity causes highly diverse transcriptional adaptations across different cell types in prefrontal cortex and striatum, suggesting brain region- and cell type-specific mechanisms contribute to pathophysiology of SCZ. Interestingly, we found the Foxp2+ neurons exhibit the most prominent gene expression changes among the different neuron subtypes in PFC, which correlate with the H3K4me3 changes. Importantly, many of the genes dysregulated in heterozygous Setd1a mice are linked to neuron morphogenesis and synaptic function. Consistently, heterozygous Setd1a mice exhibit certain behavioral features of SCZ patients. Collectively, our study establishes Setd1a heterozygous mice as a model for understanding SCZ and uncovers a complex brain region- and cell type-specific changes that potentially underlying SCZ pathogenesis. Bulk RNA-seq samples were generated from the PFC in WT and Setd+/- to study the global transcriptional changes induced by Setd1 loss. Fox2p+ PFC were FACS sorted and their transcriptome sequenced.
DNA Methyltransferase 3A Mediates the Sustained Effects of Stress on Synaptic Functions and Behaviors [RRBS]
(Rattus norvegicus)HTP Dataset Index
High-Throughput (HTP) Dataset Index metadata provided by RGD
ID: GEO:GSE147846
Tags: unclassified
Summary: Emerging evidence suggests that epigenetic mechanisms regulate aberrant gene transcription in stress-associated mental disorders. However, it remains to be elucidated about the role of DNA methylation and its catalyzing enzymes, DNA methyltransferases (DNMTs), in this process. Here we found that rats exposed to chronic (2-week) unpredictable stress exhibited a substantial reduction of Dnmt3a after stress cessation in the prefrontal cortex (PFC), a key target region of stress. Treatment of unstressed control rats with DNMT inhibitors recapitulated the effect of chronic unpredictable stress on decreased AMPAR expression and function in PFC. In contrast, overexpression of Dnmt3a in PFC of stressed animals prevented the loss of glutamatergic responses. Moreover, the stress-induced behavioral abnormalities, including the impaired recognition memory and aggressive behaviors, were ameliorated by Dnmt3a expression in PFC of stressed animals. Lastly, we found genome-wide DNA methylation changes in PFC of stressed rats are selectively enriched at several pathways, such as axon guidance, Wnt signaling and neurotransmission. These findings have therefore recognized the role of DNA epigenetic modification in stress-induced disturbance of synaptic functions and cognitive & emotional processes.
A holistic systems approach to characterize the impact of pre- and post-natal oxycodone exposure on neurodevelopment and behavior
(Rattus norvegicus)HTP Dataset Index
High-Throughput (HTP) Dataset Index metadata provided by RGD
ID: GEO:GSE159563
Tags: unclassified
Summary: RNA-sequencing of total RNA isolated from P14 PFC tissues of animals exposed to oxycodone or saline revealed alterations in the expression of key genes associated with synaptic transmission, neurodevelopment, mood disorders, and addiction in the treatment groups.
Transcription profiling by array of mouse pre-frontal cortex at different time-points after birth
(Mus musculus)HTP Dataset Index
High-Throughput (HTP) Dataset Index metadata provided by MGI
ID: ArrayExpress:E-GEOD-4675, GEO:GSE4675
Tags: baseline, age
Summary: Abnormal development of the prefrontal cortex (PFC) is associated with a number of neuropsychiatric disorders that have an onset in childhood or adolescence. Although the basic laminar structure of the PFC is established in utero, extensive remodeling continues into adolescence. To map the overall pattern of changes in cortical gene transcripts during post-natal development, we made serial measurements of mRNA levels in mouse PFC using oligonucleotide microarrays. We observed changes in mRNA transcripts consistent with known post-natal morphological and biochemical events. Overall, most transcripts that changed significantly showed a progressive decrease in abundance after birth, with the majority of change between post-natal weeks 2 and 4. Genes with cell proliferative, cytoskeletal, extracellular matrix, plasma membrane lipid / transport, protein folding, and regulatory functions had decreases in mRNA levels. Quantitative PCR verified the microarray results for six selected genes: DNA methyltransferase 3A (Dnmt3a), procollagen, type III, alpha 1 (Col3a1), solute carrier family 16 (monocarboxylic acid transporters), member 1 (Slc16a1), MARCKS-like 1 (Marcksl1), nidogen 1 (Nid1) and 3-hydroxybutyrate dehydrogenase (heart, mitochondrial) (Bdh). Keywords: time course, development, mRNA expression Single-channel affymetrix arrays were used to profile mRNA expression in the prefrontal cortex (PFC) of male mice at different time-points after birth (post-natal). Each array is an independent animal.
Early life stress leads to gene expression down-regulation in prefrontal cortex [RNA-seq]
(Rattus norvegicus)HTP Dataset Index
High-Throughput (HTP) Dataset Index metadata provided by RGD
ID: GEO:GSE153043
Tags: unclassified
Summary: Early life stress (ELS) is associated with adverse mental health outcomes including anxiety, depression and addiction-like behaviours. While ELS is known to affect the developing brain by leading to increased stress responsiveness and increased glucocorticoid levels, the molecular mechanisms underlying the detrimental effects of ELS remain incompletely characterised. Rodent models have been instrumental in beginning to uncover the molecular and cellular underpinnings of ELS. Limited nesting (LN), an ELS behavioural paradigm with significant improvements over maternal separation, mimics human maternal neglect. We have previously shown that LN leads to anxiety like-behaviours in rats. Here we assessed gene expression changes induced by ELS in rat prefrontal cortex by RNA-sequencing. We show that LN leads primarily to transcriptional repression and identify a molecular signature of LN in rat PFC that is robust to the behavioural paradigm and replicable across rodent species (mouse and rat).
Transcriptional profiling of mouse prefrontal cortex and nucleus accumbens under chronic jet lag
(Mus musculus)HTP Dataset Index
High-Throughput (HTP) Dataset Index metadata provided by MGI
ID: ArrayExpress:GSE153540
Tags: anatomical structure, baseline, time of day
Summary: Chronic jet lag (CJL) induced by shifting light-dark cycles repeatedly is a commonly used protocol to mimic the environmental light/dark changes encountered by shift workers. We conducted RNA sequencing using prefrontal cortex (PFC) and nucleus accumbens (NAc) tissues from these animals, which are brains regions strongly implicated in the pathology of various neurological and psychiatric conditions. Our results reveal the alterations of brain activities and systematic reprogramming of gene expression in brain tissues under CJL, building hypothesis for how CJL increases the susceptibility to neurological and psychiatric diseases. 8-week-old male C57BL/6J mice purchased from Model Animal Research Center of Nanjing University were assigned to different cages randomly with approximately 5 animals per cage. Animals were housed in light-tight cabinets with time-controlled illumination. Food and sterilized water were accessible ad libitum. The mice were housed under 12 hour light: 12 hour dark (12L12D) for 2 weeks for entrainment prior to CJL treatment. For CJL group, lights on and off times were advanced by 6 hours every 2 days whereas for control group they remain unchanged. On CJL Day 10, PFC and NAc were harvested from 3 control and 3 CJL treated animals at Zeitgeber Time 1 (ZT1, 1 hour after lights on; ZT0 is defined as the time of lights on) and ZT13, respectively.
HTP Dataset Index
High-Throughput (HTP) Dataset Index metadata provided by MGI
ID: ArrayExpress:E-GEOD-10784, GEO:GSE10784
Tags: WT vs. mutant, anatomical structure, genotype
Summary: This represents an unbiased evaluation of the transcriptional response in the prefrontal cortex and hippocampus areas in the Df(16)A/+ mice, a mouse model of human 22q11 microdeletion syndrome. These mice were generated by chromosomal engineering and carry a microdeltion of ~1.3Mb in the mouse locus syntenic to the human 22q11.1; The reasoning behind this expression profiling is that alterations in transcriptional programs reflect either downstream (immediate or remote) effects of the deficiency or reactive (compensatory) changes, and can thus point to affected biological processes and molecular functions. Experiment Overall Design: A total of 20 PFC and 20 HPC from 10 Df(16)A/+ mutants and 10 WT control mice was used for RNA extraction and hybridization on Affymetrix microarrays. All mice were male littermates 8 weeks of age.
Postweaning iron deficiency in rats alters reelin expression in the nucleus accumbens
(Rattus norvegicus)HTP Dataset Index
High-Throughput (HTP) Dataset Index metadata provided by RGD
ID: GEO:GSE132094
Tags: unclassified
Summary: Background: Epidemiological research indicates that iron deficiency (ID) in infancy correlates with long-term cognitive impairment and behavioral disturbances, despite therapy. However, the mechanisms underlying these effects are unknown. Objective: We investigated how ID affected postweaning behavior and monoamine concentration in rat brains to determine whether ID during the juvenile period affected gene expression and synapse formation in the prefrontal cortex (PFC) and nucleus accumbens (NAcc). Methods: Fischer344/Jcl male rats aged 21–39 days were fed low-iron diets (0.35 mg/kg iron; ID group) or standard AIN-93 G diets (3.5 mg/kg iron; control group). The locomotor activity of male offspring was evaluated by the open field and elevated plus maze tests at ages 8 and 12 weeks. Monoamine concentrations in the PFC, NAcc, caudate-putamen, ventral midbrain, dorsal midbrain, and pons were analyzed. Comprehensive gene expression analysis was performed in the PFC and NAcc at age 13 weeks. Finally, we investigated synaptic density in the PFC and NAcc by synaptophysin immunostaining. Results: Behavioral tests revealed significant interactions between age and iron consumption for the total distance traveled and the distance traveled in the peripheral area (p < 0.05), indicating that ID during the juvenile period affected hyperactivity and that this persisted to adulthood. At age 13 weeks, the ID group had increased levels of both dopamine and the metabolites of dopamine and serotonin in the NAcc. Comprehensive gene expression analysis and immunostaining showed decreased Reelin gene expression (adjusted p < 0.01) and significantly increased spine density in the NAcc in the ID group compared with the control group (p < 0.01). Conclusions: ID during the postweaning juvenile period led to long-term hyperactivity, monoamine disturbance in the brain, and downregulation of Reelin expression in the NAcc despite complete iron repletion. Epigenetic modification of Reelin genes may be involved in synaptic plasticity in the NAcc.
Early life stress leads to gene expression down-regulation in prefrontal cortex [microarray]
(Rattus norvegicus)HTP Dataset Index
High-Throughput (HTP) Dataset Index metadata provided by RGD
ID: GEO:GSE153042
Tags: unclassified
Summary: Early life stress (ELS) is associated with adverse mental health outcomes including anxiety, depression and addiction-like behaviours. While ELS is known to affect the developing brain by leading to increased stress responsiveness and increased glucocorticoid levels, the molecular mechanisms underlying the detrimental effects of ELS remain incompletely characterised. Rodent models have been instrumental in beginning to uncover the molecular and cellular underpinnings of ELS. Limited nesting (LN), an ELS behavioural paradigm with significant improvements over maternal separation, mimics human maternal neglect. We have previously shown that LN leads to anxiety like-behaviours in rats. Here we assessed gene expression changes induced by ELS in rat prefrontal cortex by RNA-sequencing. We show that LN leads primarily to transcriptional repression and identify a molecular signature of LN in rat PFC that is robust to the behavioural paradigm and replicable across rodent species (mouse and rat).
Prenatal alcohol exposure alters steady-state and activated gene expression in the adult rat brain
(Rattus norvegicus)HTP Dataset Index
High-Throughput (HTP) Dataset Index metadata provided by RGD
ID: GEO:GSE63561
Tags: unclassified
Summary: Background: Prenatal alcohol exposure (PAE) is associated with alterations in numerous physiological systems, including the stress and immune systems. We have previously shown that PAE increases the course and severity of arthritis in an adjuvant-induced arthritis (AA) model. While the molecular mechanisms underlying these effects are not fully known, changes in neural gene expression are emerging as important factors in the etiology of PAE effects. As the prefrontal cortex (PFC) and hippocampus (HPC) play key roles in neuroimmune function, PAE-induced alterations to their transcriptome may underlie abnormal steady-state functions and responses to immune challenge. The current study examined brains from adult PAE and control females from our recent AA study to determine whether PAE causes long-term alterations in gene expression and whether these mediate the altered severity and course of arthritis in PAE females Methods: Adult females from PAE, pair-fed [PF], and ad libitum-fed control [C]) groups were injected with either saline or complete Freund’s adjuvant. Animals were terminated at the peak of inflammation or during resolution (days 16 and 39 post-injection, respectively); cohorts of saline-injected PAE, PF and C females were terminated in parallel. Gene expression was analyzed in the PFC and HPC using whole genome mRNA expression microarrays. Results: Significant changes in gene expression in both the PFC and HPC were found in PAE compared to controls in response to ethanol exposure alone (saline-injected females), including genes involved in neurodevelopment, apoptosis, and energy metabolism. Moreover, in response to inflammation (adjuvant-injected females), PAE animals showed unique expression patterns, while failing to exhibit the activation of genes and regulators involved in the immune response observed in control and pair-fed animals. Conclusions: These results support the hypothesis that PAE affects neuroimmune function at the level of gene expression, demonstrating long-term effects of PAE on the CNS response under steady-state conditions and following an inflammatory insult. Key words: prenatal alcohol exposure (PAE), ethanol, inflammation, arthritis, gene expression, rat.
HTP Dataset Index
High-Throughput (HTP) Dataset Index metadata provided by MGI
ID: ArrayExpress:E-GEOD-80633, GEO:GSE80633
Tags: WT vs. mutant, genotype
Summary: To identify gene expression changes associated with Crtc1 deficiency, we performed genome-wide transcriptome profile analyses by using mouse cDNA microarrays in the cortex of Crtc1-/- and WT female mice BACKGROUND: Recent studies involve the arginine-decarboxylation product agmatine in mood regulation. Agmatine has antidepressant properties in rodent models of depression, and agmatinase (Agmat), the agmatine-degrading enzyme, is upregulated in the brain of mood disorders patients. We showed that mice lacking CREB-regulated transcription coactivator 1 (CRTC1) associate neurobehavioral and molecular depressive-like endophenotypes, as well as blunted responses to classical antidepressants. METHODS: The molecular basis of the behavioral phenotype of Crtc1-/- mice was further examined using microarray analysis. We characterized Agmat expression in the prefrontal cortex (PFC) and hippocampus (HIP) by quantitative polymerase chain reaction (qPCR), Western blot (WB) analysis, and confocal immunofluorescence microscopy. The antidepressant effect of agmatine was assessed by the forced swim test (FST). Brain-derived neurotrophic factor (BDNF) levels and eukaryotic elongation factor 2 (eEF2) phosphorylation were measured by WB. RESULTS: Microarray, qPCR and WB analyses revealed an upregulation of Agmat in Crtc1-/- PFC and HIP, where immunofluorescence microscopy showed more Agmat-expressing cells, notably parvalbumin- and somatostatin-interneurons. Acute agmatine treatment efficiently improved depressive-like behavior of Crtc1-/- mice in the FST, suggesting that exogenous agmatine has a rapid antidepressant effect through the compensation of agmatine deficit induced by upregulated Agmat. In WT mice, agmatine rapidly increased BDNF levels and eEF2 dephosphorylation, indicating that it might be a fast-acting antidepressant with NMDA receptor antagonist properties. CONCLUSIONS: Collectively, these findings support the involvement of the agmatinergic system in the depressive-like phenotype of Crtc1-/- mice, and allow a better understanding of the agmatinergic system and its putative role in major depression. RNA from cortex of 5 WT and 5 KO mice was used
Cell type-specific mechanism of Setd1a heterozygosity in schizophrenia pathogenesis [single-cell RNA-seq]
(Mus musculus)HTP Dataset Index
High-Throughput (HTP) Dataset Index metadata provided by MGI
ID: ArrayExpress:GSE181021
Tags: WT vs. mutant, anatomical structure
Summary: Schizophrenia (SCZ) is a chronic, serious mental disorder with severe burden on patients' families and society. Although over 100 genes have been linked to SCZ pathogenies, the underlying molecular and cellular mechanisms remain largely unknown. Here, we generated a Setd1a haploinsufficiency mouse model to understand how this SCZ-associated epigenetic factor affects gene expression programs in cells of brain regions highly relevant to SCZ. By comparing single-cell RNA-seq results from wild type and Setd1a+/- mice, we found Setd1a heterozygosity causes highly diverse transcriptional adaptations across different cell types in prefrontal cortex and striatum, suggesting brain region- and cell type-specific mechanisms contribute to pathophysiology of SCZ. Interestingly, we found the Foxp2+ neurons exhibit the most prominent gene expression changes among the different neuron subtypes in PFC, which correlate with the H3K4me3 changes. Importantly, many of the genes dysregulated in heterozygous Setd1a mice are linked to neuron morphogenesis and synaptic function. Consistently, heterozygous Setd1a mice exhibit certain behavioral features of SCZ patients. Collectively, our study establishes Setd1a heterozygous mice as a model for understanding SCZ and uncovers a complex brain region- and cell type-specific changes that potentially underlying SCZ pathogenesis. To mimic Setd1a loss-of-function mutations in a mouse model, we used CRISPR-Cas9 technique and targeted the 15th exon of Setd1a , which is right before the SET domain encoded by exons 16-18. we dissected PFC tissues from acute coronal sections of Setd1a+/- and WT mouse brains and dissociated the tissues to single cells, which were processed with the 10x Chromium platform (10X Genomics, CA). In additional to PFC, we performed similar scRNA-seq to analyze the transcriptional effect of Setd1a heterozygosity in striatum (including both dorsal and ventral striatum) of two WT and two Setd1a+/- mice.
HTP Dataset Index
High-Throughput (HTP) Dataset Index metadata provided by RGD
ID: GEO:GSE166095
Tags: unclassified
Summary: Background: Methamphetamine (METH) is one of the most widely abused illicit substances worldwide; unfortunately, its addiction mechanism remains unclear. Based on accumulating evidence, changes in gene expression and chromatin modifications might be related to the persistent effects of METH on the brain. In the present study, we took advantage of METH-induced behavioral sensitization as an animal model that reflects some aspects of drug addiction and examined the changes in gene expression and histone acetylation in the prefrontal cortex (PFC) of adult rats. Methods: We conducted mRNA microarray and chromatin immunoprecipitation (ChIP) coupled to DNA microarray (ChIP-chip) analyses to screen and identify changes in transcript levels and histone acetylation patterns. Functional enrichment analyses, including Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses, were performed to analyze the differentially expressed genes. We then further identified alterations in ANP32A (acidic leucine-rich nuclear phosphoprotein-32A) and POU3F2 (POU domain, class 3, transcription factor 2) using qPCR and ChIP-PCR assays. Results: In the rat model of METH-induced behavioral sensitization, METH challenge caused 275 differentially expressed genes and a number of hyperacetylated genes (821 genes with H3 acetylation and 10 genes with H4 acetylation). Based on mRNA microarray and GO and KEGG enrichment analyses, 24 genes may be involved in METH-induced behavioral sensitization, and 7 were confirmed using qPCR. We further examined the alterations in the levels of the ANP32A and POU3F2 transcripts and histone acetylation at different periods of METH-induced behavioral sensitization. H4 hyperacetylation contributed to the increased levels of ANP32A mRNA and H3/H4 hyperacetylation contributed to the increased levels of POU3F2 mRNA induced by METH challenge-induced behavioral sensitization, but not by acute METH exposure. Conclusions: The present results revealed alterations in transcription and histone acetylation in the rat PFC by METH exposure and provided evidence that modifications of histone acetylation contributed to the alterations in gene expression caused by METH-induced behavioral sensitization.
HTP Dataset Index
High-Throughput (HTP) Dataset Index metadata provided by RGD
ID: GEO:GSE166094
Tags: unclassified
Summary: Background: Methamphetamine (METH) is one of the most widely abused illicit substances worldwide; unfortunately, its addiction mechanism remains unclear. Based on accumulating evidence, changes in gene expression and chromatin modifications might be related to the persistent effects of METH on the brain. In the present study, we took advantage of METH-induced behavioral sensitization as an animal model that reflects some aspects of drug addiction and examined the changes in gene expression and histone acetylation in the prefrontal cortex (PFC) of adult rats. Methods: We conducted mRNA microarray and chromatin immunoprecipitation (ChIP) coupled to DNA microarray (ChIP-chip) analyses to screen and identify changes in transcript levels and histone acetylation patterns. Functional enrichment analyses, including Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses, were performed to analyze the differentially expressed genes. We then further identified alterations in ANP32A (acidic leucine-rich nuclear phosphoprotein-32A) and POU3F2 (POU domain, class 3, transcription factor 2) using qPCR and ChIP-PCR assays. Results: In the rat model of METH-induced behavioral sensitization, METH challenge caused 275 differentially expressed genes and a number of hyperacetylated genes (821 genes with H3 acetylation and 10 genes with H4 acetylation). Based on mRNA microarray and GO and KEGG enrichment analyses, 24 genes may be involved in METH-induced behavioral sensitization, and 7 were confirmed using qPCR. We further examined the alterations in the levels of the ANP32A and POU3F2 transcripts and histone acetylation at different periods of METH-induced behavioral sensitization. H4 hyperacetylation contributed to the increased levels of ANP32A mRNA and H3/H4 hyperacetylation contributed to the increased levels of POU3F2 mRNA induced by METH challenge-induced behavioral sensitization, but not by acute METH exposure. Conclusions: The present results revealed alterations in transcription and histone acetylation in the rat PFC by METH exposure and provided evidence that modifications of histone acetylation contributed to the alterations in gene expression caused by METH-induced behavioral sensitization.
T12D8.9
(Caenorhabditis elegans)Gene
Name: Protein PFC0760c-like
Synonyms: CELE_T12D8.9
Source: WB:WBGene00011736
Biotype: protein coding gene
(GRCh38)X:47627296G>A
(Homo sapiens)Allele/Variant
Source: rs8177076
Genes: CFP (Hsa)
Synonyms: Not Available
Variant Type: SNP
Molecular Consequence: missense_variant, non_coding_transcript_exon_variant
Diseases: Not Available
Variant Name: (GRCh38)X:47627296G>A
Gene Synonyms: PFC
(GRCh38)X:47627618C>T
(Homo sapiens)Allele/Variant
Source: rs1190480861
Genes: CFP (Hsa)
Synonyms: Not Available
Variant Type: SNP
Molecular Consequence: missense_variant, non_coding_transcript_exon_variant
Diseases: Not Available
Variant Name: (GRCh38)X:47627618C>T
Gene Synonyms: PFC
(GRCh38)X:47629630C>T
(Homo sapiens)Allele/Variant
Source: rs374687577
Genes: CFP (Hsa)
Synonyms: Not Available
Variant Type: SNP
Molecular Consequence: missense_variant, 5_prime_UTR_variant, non_coding_transcript_exon_variant
Diseases: Not Available
Variant Name: (GRCh38)X:47629630C>T
Gene Synonyms: PFC
(GRCh38)X:47627191G>A
(Homo sapiens)Allele/Variant
Source: rs200036265
Genes: CFP (Hsa)
Synonyms: Not Available
Variant Type: SNP
Molecular Consequence: missense_variant, non_coding_transcript_exon_variant
Diseases: Not Available
Variant Name: (GRCh38)X:47627191G>A
Gene Synonyms: PFC
(GRCh38)X:47629677G>A
(Homo sapiens)Allele/Variant
Source: rs918926806
Genes: CFP (Hsa)
Synonyms: Not Available
Variant Type: SNP
Molecular Consequence: splice_region_variant, non_coding_transcript_variant, intron_variant
Diseases: Not Available
Variant Name: (GRCh38)X:47629677G>A
Gene Synonyms: PFC
(GRCh38)X:47629803C>T
(Homo sapiens)Allele/Variant
Source: rs371398463
Genes: CFP (Hsa)
Synonyms: Not Available
Variant Type: SNP
Molecular Consequence: 5_prime_UTR_variant, non_coding_transcript_exon_variant, synonymous_variant
Diseases: Not Available
Variant Name: (GRCh38)X:47629803C>T
Gene Synonyms: PFC
(GRCh38)X:47629827C>T
(Homo sapiens)Allele/Variant
Source: rs1020912849
Genes: CFP (Hsa)
Synonyms: Not Available
Variant Type: SNP
Molecular Consequence: 5_prime_UTR_variant, non_coding_transcript_exon_variant, synonymous_variant
Diseases: Not Available
Variant Name: (GRCh38)X:47629827C>T
Gene Synonyms: PFC