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Genome-wide chromatin-immunoprecipitation studies of sympathetic neurons reveals critical direct targets of ISL1 and suggests potential co-factor families for ISL1 action in sympathetic neurons

ABSTRACT: Understanding factors that drive development of the sympathetic neuron is crucial to development of potential therapies for neuroblastoma. Here, we identify a key cell autonomous role for the LIM homeodomain transcription factor ISL1 for survival, proliferation and differentiation of sympathetic neurons throughout development. Chromatin immunoprecipitation assays performed utilizing antibody to ISL1 in chromatin extracts from sympathetic neurons demonstrated that ISL1 directly binds genomic regions within several genes critical for sympathetic neuron development and function, including subunits of the Insm1, Lmo1,Tlx3 and Prox1. Our studies represent in vivo ChIP-seq studies for sympathetic neurons which provide a basis for further exploration of factors critical to sympathetic neurons development and function .

ORGANISM(S): Mus musculus

PROVIDER: GSE93304 | GEO | 2017/11/09

SECONDARY ACCESSION(S): PRJNA360584

REPOSITORIES: GEO

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Genome-wide mRNA expression analyses revealed dysregulation of genes important for sympathetic neuron development in isl1 cko and hypomorphic mutant embryos.

Project description:Understanding factors that drive development and function of the sympathetic neuron is crucial to development of potential therapies for neuroblastoma. Here, we identify a key cell autonomous role for the LIM homeodomain transcription factor ISL1 for survival, proliferation and differentiation of sympathetic neurons throughout development. Analysis of several Isl1 mutant mouse lines, including one in which Isl1 was specifically ablated in sympathetic neuron (Wnt1-cre;Isl1 f/f) revealed an early requirement for Isl1 within sympathetic neurons for proliferation and surrvial. RNA-seq analyses on sympathetic neurons revealed dysregulation of a number of genes critical for sympathetic neuron development .Our studies demonstrated that ISL1 regulated the peoliferation, surrvial and differentiation.

2017-11-09 | GSE93306 | GEO

Functional Connection with Cardiac Tissues Confers Maturation Phenotypes in hPSC-Derived PHOX2B::GFP Expressing Sympathetic Neurons

Project description:Neurons derived from human pluripotent stem cells (hPSCs) are a remarkable tool for modeling human neural development and diseases. However, it remains largely unknown whether the hPSC-derived neurons can be functionally coupled with their target tissues in vitro, which is essential for understanding inter-cellular physiology and further translational studies. Here, we demonstrate that hPSC-derived sympathetic neurons can be obtained from hPSCs and that the resulting neurons form physical and functional connections with cardiac muscle cells. By use of multiple hPSC reporter lines, we recapitulated human autonomic neuron development in vitro, and successfully isolated PHOX2B::eGFP+ neurons exhibiting sympathetic marker expression, electrophysiological properties, and norepinephrine secretion. With pharmacological and optogenetic manipulations, the PHOX2B::eGFP+ neurons controlled the beating rates of cardiomyocytes, and their physical interaction led to neuronal maturation. Our study lays a foundation for the specification of human sympathetic neurons and for the hPSC-based neuronal control of end organs in a dish. Using the four genetic reporter systems (OCT4::eGFP, SOX10::eGFP, ASCL1::eGFP, and PHOX2B::eGFP reporter hESC lines), we were able to purify discrete cell populations at four differentiation stages, recapitulating the sympathoadrenal differentiation process in vitro with purified and defined populations in four specific differentiation stages. We performed transcriptome analysis of OCT4::eGFP+ cells (3 biological replicates, representing undifferentiated hESCs), SOX10::eGFP+ cells (3 biological replicates, multi-potent neural crest), ASCL1::eGFP+ cells (3 biological replicates, putative sympathoadrenal progenitors), and PHOX2B::eGFP+ cells (2 biological replicates, putative sympathetic neuronal precursors).

2016-07-01 | E-GEOD-80689 | biostudies-arrayexpress

Functional Connection with Cardiac Tissues Confers Maturation Phenotypes in hPSC-Derived PHOX2B::GFP Expressing Sympathetic Neurons

2016-07-01 | GSE80689 | GEO

ISL1 and POU4F1 directly interact to regulate the differentiation and survival of inner ear sensory neurons

Project description:The inner ear sensory neurons play a pivotal role in auditory processing and balance control. Though significant progresses have been made, the underlying mechanisms controlling the differentiation and survival of the inner ear sensory neurons remain largely unknown. During development, ISL1 and POU4F transcription factors are co-expressed and are required for terminal differentiation, pathfinding, axon outgrowth and the survival of neurons in the central and peripheral nervous systems. However, little is understood about their functional relationship and regulatory mechanism in neural development. Here, we have knocked out Isl1 or Pou4f1 or both in mice of both sexes. In the absence of Isl1, the differentiation of cochleovestibular ganglion (CVG) neurons is disturbed and with that Isl1-deficient CVG neurons display defects in migration and axon pathfinding. Compound deletion of Isl1 and Pou4f1 causes a delay in CVG differentiation and results in a more severe CVG defect with a loss of nearly all of spiral ganglion neurons (SGNs). Moreover, ISL1 and POU4F1 interact directly in developing CVG neurons and act cooperatively as well as independently in regulating the expression of unique sets of CVG-specific genes crucial for CVG development and survival by binding to the cis-regulatory elements including the promoters of Fgf10, Pou4f2, and Epha5 and enhancers of Eya1 and Ntng2 These findings demonstrate that Isl1 and Pou4f1 are indispensable for CVG development and maintenance by acting epistatically to regulate genes essential for CVG development.

2024-05-31 | GSE233706 | GEO

Transcription profiling of mouse sympathetic neurons cultured alone and in contact with their myocyte targets

Project description:We identified 112 known genes and 150 expressed sequence tags (ESTs) showing more than a 1.3 fold change in target-exposed neurons compared to neurons grown in the absence of target. Expression of 36 genes and 49 ESTs was upregulated, while expression of 76 genes and 101 ESTs was downregulated by the presence of target during the culture period. Overall, these changes represented approximately 1.6% of the probe set. Experiment Overall Design: We investigated the molecular basis of the target-regulated growth inhibition program using DNA microarrays to analyze patterns of gene expression following contact of sympathetic neurons with their myocyte targets. Total RNA was isolated from sympathetic neurons cultured alone and from neurons isolated from myocyte co-cultures. The two neuron populations showed minimal levels of atrial natriutic peptide (ANF) mRNA, a myocyte marker, compared to myocyte-containing cultures, indicating a low level of myocyte contamination for neurons purified from co-cultures. Experiment Overall Design: Isolated total RNA was reverse transcribed, labeled with biotin by in vitro transcription and hybridized to an Affymetrix Rat Expression Set 230A microarray with 15,900 probe sets. The hybridized microarray was washed, stained, scanned and quantified using DNA-Chip Analyzer (dChip) 1.3 (Li and Wong, 2001).

2008-06-16 | E-GEOD-8393 | biostudies-arrayexpress

Neural crest origin of sympathetic neurons at the dawn of vertebrates

Project description:he neural crest is an embryonic stem cell population unique to vertebrates whose expansion and diversification are thought to have promoted vertebrate evolution by enabling emergence of novel cell types and structures like jaws and peripheral ganglia2. While basal vertebrates have sensory ganglia, convention has it that trunk sympathetic chain ganglia arose only in jawed vertebrates. In contrast, here we report the presence of trunk sympathetic neurons in the sea lamprey, Petromyzon marinus, an extant jawless vertebrate. These neurons arise from sympathoblasts near the dorsal aorta that undergo noradrenergic specification via a transcriptional program homologous to that described in gnathostomes. Lamprey sympathoblasts populate the extracardiac space and extend along the length of the trunk in bilateral streams, expressing the catecholamine biosynthetic pathway enzymes tyrosine hydroxylase and dopamine -hydroxylase. CM-DiI lineage tracing analysis further confirmed that these cells derive from the trunk neural crest. RNA-seq of isolated ammocete trunk sympathoblasts revealed gene profiles characteristic of sympathetic neuron function. Our findings challenge prevailing dogma which posits that sympathetic ganglia are a gnathostome innovation, instead suggesting that a late-developing rudimentary sympathetic nervous system may have been characteristic of the earliest vertebrates.

2024-02-22 | GSE246248 | GEO

Gene expression analysis of SCG sympathetic neurons with loss of Egr3

Project description:The transcription factor Egr3 has been shown to have a cell autonomous role in sympathetic nervous system (SNS) development. We utilized microarray analysis to identify potential downstream target genes deregulated with loss of Egr3. Both conditions were in the null Bax background to prevent apoptosis and therefore mitigate identification of apoptosis related genes. Our analysis identified genes involved in biological processes that were expected such as SNS development and axonogenesis as well as those that were unexpected such as dendritogenesis and axon guidance. This led us to investigate whether Egr3 is important in these unexpected biological processes within sympathetic neurons. Total RNA was obtained from superior cervical ganglion (SCG) dissected from P0 mice with the genotype of Egr3+/+; Bax-/- or Egr3-/-; Bax-/-. Each genotype had 3 samples each.

2013-03-22 | E-GEOD-41290 | biostudies-arrayexpress

Genome-wide studies of sympathetic neuron development

Project description:Genome-wide studies of sympathetic neuron development

| PRJNA360582 | ENA

Transcriptional responses of sympathetic neurons during BMP-induced primary dendritogenesis

Project description:The objective of this study was to identify genes that are differentially regulated in cultured sympathetic neurons during BMP-induced dendritic growth and to determine the temporal expression patterns of these genes. We determined that inhibiting transcription within the first 24 hours after adding exogenous BMP-7 blocks BMP-induced dendritic growth in cultured sympathetic neurons dissociated from the superior cervical ganglia of embryonic rat pups. Thus, we determined the transcriptional profiles of cultured sympathetic neurons at 6 and 24 hours after addition of BMP-7 to identify early and later transcriptional responses that may drive dendrite formation. We isolated total RNA from sympathetic neurons exposed to three different experimental conditions: (1) no BMP-7 treatment; (2) treatment with BMP-7 for 6 hours; and (3) treatment with BMP-7 for 24 hours. Total RNA was labeled and hybridized to Affymetrix Rat Genome U34A oligonucleotide microarrays. This experiment was independently repeated three times using cultures derived from three independent dissections, such that a total of nine arrays were used. The nine samples were processed over two batches and the batching was balanced across the treatment conditions. Image data was processed using Affymetrix GCOS software to generate numeric, probe level data (CEL) and CEL data was then pre-processed using the RMA algorithm implemented by Partek Genomics Suite (St. Louis, MO). Following batch correction of the probe set level, normalized data using Partek, differential gene expression was determined by two-way ANOVA and linear contrasts between all treatment conditions were applied to generate fold-change values along with the statistical p-value. Lists of significantly changed transcripts were uploaded to MetaCore (GeneGo, ) for mining biological annotation and network analysis.

2011-06-30 | E-GEOD-28150 | biostudies-arrayexpress

Microbes modulate sympathetic neurons via a gut-brain circuit

Project description:Gut-brain connections monitor the intestinal tissue and its microbial and dietary content1, regulating both intestinal physiological functions such as nutrient absorption and motility2,3, and brain–wired feeding behaviour2. It is therefore plausible that circuits exist to detect gut microbes and relay this information to central nervous system (CNS) areas that, in turn, regulate gut physiology4. We characterized the influence of the microbiota on enteric–associated neurons (EAN) by combining gnotobiotic mouse models with transcriptomics, circuit–tracing methods, and functional manipulation. We found that the gut microbiome modulates gut–extrinsic sympathetic neurons; while microbiota depletion led to increased cFos expression, colonization of germ-free mice with short-chain fatty acid–producing bacteria suppressed cFos expression in the gut sympathetic ganglia. Chemogenetic manipulations, translational profiling, and anterograde tracing identified a subset of distal intestine-projecting vagal neurons positioned to play an afferent role in microbiota–mediated modulation of gut sympathetic neurons. Retrograde polysynaptic neuronal tracing from the intestinal wall identified brainstem sensory nuclei activated during microbial depletion, as well as efferent sympathetic premotor glutamatergic neurons that regulate gastrointestinal transit. These results reveal microbiota–dependent control of gut extrinsic sympathetic activation through a gut-brain circuit.

2020-03-20 | GSE145986 | GEO

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