scholarly journals Information-dependent Enrichment Analysis Reveals Time-dependent Transcriptional Regulation of the Estrogen Pathway of Toxicity

2016 ◽  
Author(s):  
Salil N. Pendse ◽  
Alexandra Maertens ◽  
Michael Rosenberg ◽  
Dipanwita Roy ◽  
Rick A. Fasani ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Transcription Factors ◽  
Expression Patterns ◽  
Enrichment Analysis ◽  
Fold Change ◽  
Gene Set Enrichment Analysis ◽  
High Dose ◽  
Functional Responses ◽  
Pathways Of Toxicity

The twenty-first century vision for toxicology involves a transition away from high-dose animal studies and into in vitro and computational models. This movement requires mapping pathways of toxicity through an understanding of how in vitro systems respond to chemical perturbation. Uncovering transcription factors responsible for gene expression patterns is essential for defining pathways of toxicity, and ultimately, for determining chemical mode of action, through which a toxicant acts. Traditionally this is achieved via chromatin immunoprecipitation studies and summarized by calculating, which transcription factors are statistically associated with the up- and down-regulated genes. These lists are commonly determined via statistical or fold-change cutoffs, a procedure that is sensitive to statistical power and may not be relevant to determining transcription factor associations. To move away from an arbitrary statistical or fold-change based cutoffs, we have developed in the context of the Mapping the Human Toxome project, a novel enrichment paradigm called Information Dependent Enrichment Analysis (IDEA) to guide identification of the transcription factor network. We used the test case of endocrine disruption of MCF-7 cells activated by 17β estradiol (E2). Using this new approach, we were able to establish a time course for transcriptional and functional responses to E2. ERα and ERβ are associated with short-term transcriptional changes in response to E2. Sustained exposure leads to the recruitment of an additional ensemble of transcription factors and alteration of cell-cycle machinery. TFAP2C and SOX2 were the transcription factors most highly correlated with dose. E2F7, E2F1 and Foxm1, which are involved in cell proliferation, were enriched only at 24h. IDEA is, therefore, a novel tool to identify candidate pathways of toxicity, clearly outperforming Gene-set Enrichment Analysis but with similar results as Weighted Gene Correlation Network Analysis, which helps to identify genes not annotated to pathways.

scholarly journals Transcriptome profilings reveal the candidate genes, pathways and transcription factors related to nitrogen utilization and excessive nitrogen stress in perennial ryegrass.

2020 ◽  
Author(s):  
Yinruizhi Li ◽  
Mengdi Wang ◽  
Ke Teng ◽  
Di Dong ◽  
Zhuocheng Liu ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Transcription Factors ◽  
Perennial Ryegrass ◽  
Expression Patterns ◽  
Enrichment Analysis ◽  
Nitrogen Utilization ◽  
Utilization Rate ◽  
Nitrogen Stress ◽  
Molecular Response ◽  
Stress Effect

Abstract Background：Lolium perenne L. is a kind of high quality forage grass, which can provide a good nutritional basis for herbivorous livestock. However, how to improve the nitrogen utilization rate of ryegrass and avoid the nitrate toxicity caused by excessive nitrogen has been troubling people for a long time. Up to now, the molecular response mechanism of ryegrass to nitrogen is not clear, especially under the condition of excessive nitrogen. Based on this, we tried to obtain a new insight into molecular response of ryegrass in nitrogen utilization and excessive nitrogen stress, providing the molecular theoretical basis for solving this problem.Results: In this study, the transcription of perennial ryegrass at different nitrogen levels was identified by high-throughput next-generation DNA sequencing. Phenotypic characterizations investigated that ryegrass in treatment N0.5 has a better growth state than the other three groups. The treatment N1 and N10 contained excessive nitrogen, which had a stress effect on plant growth. Analysis of differentially expressed genes indicated that 345, 105 genes are considered to involve in the regulation of nitrogen utilization and excessive nitrogen stress, respectively. GO enrichment analysis revealed that plant response to nitrogen mainly enrich in two categories, including “biological process” and “molecular function”. KEGG enrichment analysis suggested that “Photosynthesis-antenna proteins” may respond positively to nitrogen under appropriate nitrogen conditions, whereas “steroid biosynthesis”, “carotenoid biosynthesis” and “C5-branched dibasic acid metabolism” had been identified as top significant enrichment pathways response to excessive nitrogen. Transcription factors analysis showed that 21 TFs related to nitrogen utilization were classified into 10 transcription factor families, especially AP2-EREBP and MYB TF families. 4 TFs related to excessive nitrogen stress were identified, which belonged to 4 transcription factor families including LOB, NAC, AP2-EREBP and HB. The expression patterns of these selected genes above were also analyzed. Conclusions: These results made a contribution to comprehend the molecular mechanism of perennial ryegrass response to nitrogen. It provides new ideas for guiding the production practice and variety improvement of forage and even food crops from the perspective of molecular biology.

scholarly journals Gene expression patterns in synchronized islet populations

2018 ◽  
Author(s):  
Nikita Mukhitov ◽  
Michael G. Roper
Keyword(s):  
Gene Expression ◽  
Environmental Changes ◽  
Expression Patterns ◽  
Enrichment Analysis ◽  
Protein Translation ◽  
Gene Set Enrichment Analysis ◽  
Gene Expression Patterns ◽  
Insulin Synthesis

AbstractIn vivo levels of insulin are oscillatory with a period of ~5-10 minutes, implying that the numerous islets of Langerhans within the pancreas are synchronized. While the synchronizing factors are still under investigation, one result of this behavior is expected to be coordinated intracellular [Ca2+] ([Ca2+]i) oscillations throughout the islet population. The role that coordinated [Ca2+]i oscillations have on controlling gene expression within pancreatic islets was examined by comparing gene expression levels in islets that were synchronized using a low amplitude glucose wave and an unsynchronized population. The [Ca2+]i oscillations in the synchronized population were homogeneous and had a significantly lower drift in their oscillation period as compared to unsynchronized islets. This reduced drift in the synchronized population was verified by comparing the drift of in vivo and in vitro profiles from published reports. Microarray profiling indicated a number of Ca2+-dependent genes were differentially regulated between the two islet populations. Gene set enrichment analysis revealed that the synchronized population had reduced expression of gene sets related to protein translation, protein turnover, energy expenditure, and insulin synthesis, while those that were related to maintenance of cell morphology were increased. It is speculated that these gene expression patterns in the synchronized islets results in a more efficient utilization of intra-cellular resources and response to environmental changes.

scholarly journals A Sclerotinia sclerotiorum Transcription Factor Involved in Sclerotial Development and Virulence on Pea

mSphere ◽  
2019 ◽  
Vol 4 (1) ◽  
Author(s):  
Hyunkyu Sang ◽  
Hao-Xun Chang ◽  
Martin I. Chilvers
Keyword(s):  
Transcription Factor ◽  
Transcription Factors ◽  
Sclerotinia Sclerotiorum ◽  
Culture Medium ◽  
Expression Patterns ◽  
White Mold ◽  
In Planta ◽  
Content Type ◽  
Sclerotial Development

ABSTRACT Sclerotinia sclerotiorum is a plant-pathogenic ascomycete fungus and infects over 400 host plants, including pea (Pisum sativum L.). The fungus causes white mold on pea, and substantial yield loss is attributed to the disease. To improve white mold management, further understanding of S. sclerotiorum pathogenicity is crucial. In this study, 389 transcription factors (TFs) were mined from the complete genome sequence of S. sclerotiorum and their in planta expression patterns were determined in susceptible and partially resistant pea lines and compared to in vitro expression patterns on culture medium. One of the transcription factors was significantly induced in planta at 24 and 48 h postinfection compared to the expression in vitro. This putative C6 transcription factor of S. sclerotiorum (SsC6TF1) was knocked down using a gene-silencing approach to investigate its functions in vegetative growth and sclerotial development as well as its virulence and pathogenicity in pea. While the SsC6TF1 knockdown mutants had hyphal growth rates identical to those of the wild-type strain and were capable of infection, the knockdown mutants produced no sclerotia or significantly fewer and smaller sclerotia on the culture medium and exhibited reduced virulence on both pea lines. This study profiled genome-wide expression for S. sclerotiorum transcription factors in planta and in vitro and functionally characterized a novel transcription factor, SsC6TF1, which positively regulates sclerotial development and virulence on pea. The finding provides molecular insights into S. sclerotiorum biology and interaction with pea and other economically important crops. IMPORTANCE White mold, caused by Sclerotinia sclerotiorum, is a destructive disease on important legume species such as soybean, dry bean, and pea. This study investigated expression levels of transcription factors in S. sclerotiorum in planta (pea lines) and in vitro (culture medium). One transcription factor displaying high expression in planta was found to be involved in sclerotial development and virulence on pea. This report provides a new understanding regarding transcription factors of S. sclerotiorum in development and virulence.

scholarly journals A hypothesis-driven approach to assessing significance of differences in RNA expression levels among specific groups of genes

2017 ◽  
Author(s):  
Mingze He ◽  
Peng Liu ◽  
Carolyn J. Lawrence-Dill
Keyword(s):  
Gene Expression ◽  
Transcription Factor ◽  
Heat Shock ◽  
Expression Patterns ◽  
Enrichment Analysis ◽  
Gene Set Enrichment Analysis ◽  
Specific Gene ◽  
Simple Method ◽  
Expression Levels ◽  
Gene Set

AbstractGenome-wide molecular gene expression studies generally compare expression values for each gene across multiple conditions followed by cluster and gene set enrichment analysis to determine whether differentially expressed genes are enriched in specific biochemical pathways, cellular components, biological processes, and/or molecular functions, etc. This approach to analyzing differences in gene expression enables discovery of gene function, but is not useful to determine whether pre-defined groups of genes share or diverge in their expression patterns in response to treatments nor to assess the correctness of pre-defined gene set groupings. Here we present a simple method that changes the dimension of comparison by treating genes as variable traits to directly assess significance of differences in expression levels among pre-defined gene groups. Because expression distributions are typically skewed (thus unfit for direct assessment using Gaussian statistical methods) our method involves transforming expression data to approximate a normal distribution followed by dividing the genes into groups, then applying Gaussian parametric methods to assess significance of observed differences. This method enables the assessment of differences in gene expression distributions within and across samples, enabling hypothesis-based comparison among groups of genes. We demonstrate this method by assessing the significance of specific gene groups’ differential response to heat stress conditions in maize.AbbreviationsGO– gene ontology HSP – heat shock proteinKEGG– Kyoto Encyclopedia of Genes and GenomesHSF TF– heat shock factor transcription factorHSBP– heat shock binding proteinRNA– ribonucleic acidTE– transposable elementTF– transcription factorTPM– transcripts per kilobase millions

scholarly journals AB0166 IMMUNOGLOBULIN G DERIVED FROM PATIENTS WITH SYSTEMIC SCLEROSIS IMPRINTS A PRO-INFLAMMATORY AND PRO-FIBROTIC PHENOTYPE IN MONOCYTE-LIKE THP-1 CELLS

2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 1383.2-1383
Author(s):  
A. Dalmann ◽  
S. Murthy ◽  
M. Wannick ◽  
G. Eleftheriadis ◽  
A. Müller ◽  
...  
Keyword(s):  
Transcription Factors ◽  
Systemic Sclerosis ◽  
Cell Line ◽  
Robust Regression ◽  
Enrichment Analysis ◽  
Gene Set Enrichment Analysis ◽  
Receptor Type ◽  
Endothelin Receptor ◽  
Angiotensin Ii Receptor

Background:Regulatory IgG autoantibodies directed against diverse G protein-coupled receptors (GPCR),i.e.antibodies with agonistic or antagonistic activity are abundant in human serum. The serum titers of autoantibodies targeting angiotensin II receptor 1 (AT1) and endothelin receptor A (ETA) are specifically altered in autoimmune diseases such as systemic sclerosis (SSc). Disease-promoting mechanisms regulated by anti-AT1and anti-ETAIgG are still elusive, but induction of pro-inflammatory and pro-fibrotic chemokines (CXCL8, CCL18) has been suggested to be one of them.Objectives:To determine the cytokine and phospho-kinase profiles induced in monocyte-like cells by IgG derived from SSc patients (SSc-IgG) enriched with anti-AT1and anti-ETAantibodies in comparison to IgG derived from healthy donors (IgG-HD).Methods:A monocyte-like cell line (THP-1) was culturedin vitroand stimulated with IgG (1 mg/ml) derived from SSc patients or HD in the presence of various inhibitors/blockers for 24h. Then, supernatants were analyzed by a human cytokine/chemokine array. Data were analyzed using bio-mathematical tools such as generalized t-test including the robust regression method from R/Bioconductor package LIMMA. In addition, THP-1 cells were culturedin vitroand stimulated with IgG (1 mg/ml) derived from SSc patients or HD for up to 30 minutes. Thereafter, cell lysates were assayed for the kinome employing a human phospho-kinase array. To validate potential effects of transcription factor inhibition, release of CXCL8 and CCL18 into the supernatant was measured by Elisa.Results:In general, SSc-IgG induced the release of most cytokines by THP-1 cells more pronouncedly than HD-IgG. The bio-mathematical analysis suggested that stimuli, responsible for the shift of the THP-1 cell cytokine profile, are more abundant in SSc-IgG than in HD-IgG. Based upon these findings a gene set enrichment analysis for transcription factors yielded the transcription factors NF-κB, AP-1, and PRDM1 (Blimp-1) as putative major regulatory hubs for the response of THP-1 cells to SSc-IgG. Further, SSc-IgG altered the phosphorylation status of several proteins, indicative of an involvement of MAPK and/or JAK/STAT pathways. Interestingly, a role for AP-1 was also proposed by the inhibition of CXCL8 and CCL18 release following pretreatment of THP-1 cells with an AP-1 blocker.Conclusion:Herein, we demonstrate that IgG of SSc patients, enriched with anti-AT1and anti-ETAautoantibodies drives THP-1 cells towards a general pro-inflammatory and pro-fibrotic phenotype, which is reflected by broad changes in the secretome and kinome of these cells. Furthermore, our results highlight AP-1 as critical regulator of gene transcription of CXCL8 and CCL18 in a monocyte-like cell line.References:[1]Cabral-Marques O, Marques A, Giil LM, De Vito R, Rademacher J, Günther J, Lange T, Humrich JY, Klapa S, Schinke S, et al. GPCR-specific autoantibody signatures are associated with physiological and pathological immune homeostasis.Nat Commun(2018)9:5224. doi:10.1038/s41467-018-07598-9[2]Günther J, Kill A, Becker MO, Heidecke H, Rademacher J, Siegert E, Radi M, Burmester G-R, Dragun D, Riemekasten G. Angiotensin receptor type 1 and endothelin receptor type A on immune cells mediate migration and the expression of IL-8 and CCL18 when stimulated by autoantibodies from systemic sclerosis patients.Arthritis Res Ther(2014)16:R65. doi:10.1186/ar4503Disclosure of Interests:Anja Dalmann: None declared, Sripriya Murthy: None declared, Melanie Wannick: None declared, Georgios Eleftheriadis: None declared, Antje Müller: None declared, Detlef Zillikens: None declared, Hauke Busch: None declared, Christian Sadik: None declared, Gabriela Riemekasten Consultant of: Cell Trend GmbH, Janssen, Actelion, Boehringer Ingelheim, Speakers bureau: Actelion, Novartis, Janssen, Roche, GlaxoSmithKline, Boehringer Ingelheim, Pfizer

Subnuclear compartmentalization of sequence-specific transcription factors and regulation of eukaryotic gene expression

2005 ◽  
Vol 83 (4) ◽  
pp. 535-547 ◽  
Author(s):  
Gareth N Corry ◽  
D Alan Underhill
Keyword(s):  
Gene Expression ◽  
Transcription Factor ◽  
Transcription Factors ◽  
Transcriptional Activation ◽  
Current Knowledge ◽  
Nuclear Architecture ◽  
Subnuclear Localization ◽  
Modular Structures

To date, the majority of the research regarding eukaryotic transcription factors has focused on characterizing their function primarily through in vitro methods. These studies have revealed that transcription factors are essentially modular structures, containing separate regions that participate in such activities as DNA binding, protein–protein interaction, and transcriptional activation or repression. To fully comprehend the behavior of a given transcription factor, however, these domains must be analyzed in the context of the entire protein, and in certain cases the context of a multiprotein complex. Furthermore, it must be appreciated that transcription factors function in the nucleus, where they must contend with a variety of factors, including the nuclear architecture, chromatin domains, chromosome territories, and cell-cycle-associated processes. Recent examinations of transcription factors in the nucleus have clarified the behavior of these proteins in vivo and have increased our understanding of how gene expression is regulated in eukaryotes. Here, we review the current knowledge regarding sequence-specific transcription factor compartmentalization within the nucleus and discuss its impact on the regulation of such processes as activation or repression of gene expression and interaction with coregulatory factors.Key words: transcription, subnuclear localization, chromatin, gene expression, nuclear architecture.

scholarly journals TNF-α Triggers RIP1/FADD/Caspase-8-Mediated Apoptosis of Astrocytes and RIP3/MLKL-Mediated Necroptosis of Neurons Induced by Angiostrongylus cantonensis Infection

2021 ◽  
Author(s):  
Hongli Zhou ◽  
Minyu Zhou ◽  
Yue Hu ◽  
Yanin Limpanon ◽  
Yubin Ma ◽  
...  
Keyword(s):  
Cell Death ◽  
Enrichment Analysis ◽  
Angiostrongylus Cantonensis ◽  
Gene Set Enrichment Analysis ◽  
Caspase 8 ◽  
Cns Injury ◽  
Vitro Assay ◽  
Tnf Α

AbstractAngiostrongylus cantonensis (AC) can cause severe eosinophilic meningitis or encephalitis in non-permissive hosts accompanied by apoptosis and necroptosis of brain cells. However, the explicit underlying molecular basis of apoptosis and necroptosis upon AC infection has not yet been elucidated. To determine the specific pathways of apoptosis and necroptosis upon AC infection, gene set enrichment analysis (GSEA) and protein–protein interaction (PPI) analysis for gene expression microarray (accession number: GSE159486) of mouse brain infected by AC revealed that TNF-α likely played a central role in the apoptosis and necroptosis in the context of AC infection, which was further confirmed via an in vivo rescue assay after treating with TNF-α inhibitor. The signalling axes involved in apoptosis and necroptosis were investigated via immunoprecipitation and immunoblotting. Immunofluorescence was used to identify the specific cells that underwent apoptosis or necroptosis. The results showed that TNF-α induced apoptosis of astrocytes through the RIP1/FADD/Caspase-8 axis and induced necroptosis of neurons by the RIP3/MLKL signalling pathway. In addition, in vitro assay revealed that TNF-α secretion by microglia increased upon LSA stimulation and caused necroptosis of neurons. The present study provided the first evidence that TNF-α was secreted by microglia stimulated by AC infection, which caused cell death via parallel pathways of astrocyte apoptosis (mediated by the RIP1/FADD/caspase-8 axis) and neuron necroptosis (driven by the RIP3/MLKL complex). Our research comprehensively elucidated the mechanism of cell death after AC infection and provided new insight into targeting TNF-α signalling as a therapeutic strategy for CNS injury.

scholarly journals Ligand-dependent repression of the erythroid transcription factor GATA-1 by the estrogen receptor.

1995 ◽  
Vol 15 (6) ◽  
pp. 3147-3153 ◽  
Author(s):  
G A Blobel ◽  
C A Sieff ◽  
S H Orkin
Keyword(s):  
Bone Marrow ◽  
Estrogen Receptor ◽  
Transcription Factor ◽  
Progenitor Cells ◽  
Erythroid Cell ◽  
High Dose ◽  
Dependent Manner ◽  
Erythroid Progenitor ◽  
Erythroid Progenitor Cells

High-dose estrogen administration induces anemia in mammals. In chickens, estrogens stimulate outgrowth of bone marrow-derived erythroid progenitor cells and delay their maturation. This delay is associated with down-regulation of many erythroid cell-specific genes, including alpha- and beta-globin, band 3, band 4.1, and the erythroid cell-specific histone H5. We show here that estrogens also reduce the number of erythroid progenitor cells in primary human bone marrow cultures. To address potential mechanisms by which estrogens suppress erythropoiesis, we have examined their effects on GATA-1, an erythroid transcription factor that participates in the regulation of the majority of erythroid cell-specific genes and is necessary for full maturation of erythrocytes. We demonstrate that the transcriptional activity of GATA-1 is strongly repressed by the estrogen receptor (ER) in a ligand-dependent manner and that this repression is reversible in the presence of 4-hydroxytamoxifen. ER-mediated repression of GATA-1 activity occurs on an artificial promoter containing a single GATA-binding site, as well as in the context of an intact promoter which is normally regulated by GATA-1. GATA-1 and ER bind to each other in vitro in the absence of DNA. In coimmunoprecipitation experiments using transfected COS cells, GATA-1 and ER associate in a ligand-dependent manner. Mapping experiments indicate that GATA-1 and the ER form at least two contacts, which involve the finger region and the N-terminal activation domain of GATA-1. We speculate that estrogens exert effects on erythropoiesis by modulating GATA-1 activity through protein-protein interaction with the ER. Interference with GATA-binding proteins may be one mechanism by which steroid hormones modulate cellular differentiation.

Transmembrane p24 Trafficking Protein 2 Regulates Inflammation Through the TLR4/NF-κB Signaling Pathway in Lung Adenocarcinoma

2021 ◽  
Author(s):  
Longhua Feng ◽  
Pengjiang Cheng ◽  
Zhengyun Feng ◽  
Xiaoyu Zhang
Keyword(s):  
Lung Adenocarcinoma ◽  
Signaling Pathway ◽  
Enrichment Analysis ◽  
Gene Set Enrichment Analysis ◽  
Inflammatory Factors ◽  
Normal Tissues ◽  
Kaplan Meier ◽  
New Strategy

Abstract Background: To investigate the role of transmembrane p24 trafficking protein 2 (TMED2) in lung adenocarcinoma (LUAD) and determine whether TMED2 knockdown could inhibit LUAD in vitro and in vivo.Methods: TIMER2.0, Kaplan-Meier plotter, gene set enrichment analysis (GSEA), Target Gene, and pan-cancer systems were used to predict the potential function of TMED2. Western blotting and immunohistochemistry were performed to analyze TMED2 expression in different tissues or cell lines. The proliferation, development, and apoptosis of LUAD were observed using a lentivirus-mediated TMED2 knockdown. Bioinformatics and western blot analysis of TMED2 against inflammation via the TLR4/NF-κB signaling pathway were conducted. Results: TMED2 expression in LUAD tumor tissues was higher than that in normal tissues and positively correlated with poor survival in lung cancer and negatively correlated with apoptosis in LUAD. The expression of TMED2 was higher in tumors or HCC827 cells. TMED2 knockdown inhibited LUAD development in vitro and in vivo and increased the levels of inflammatory factors via the TLR4/NF-κB signaling pathway. TMED2 was correlated with TME, immune score, TME-associated immune cells, their target markers, and some mechanisms and pathways, as determined using the TIMER2.0, GO, and KEGG assays.Conclusions: TMED2 may regulate inflammation in LUAD through the TLR4/NF-κB signaling pathway, and enhance the proliferation, development, and prognosis of LUAD by regulating inflammation, which provide a new strategy for treating LUAD by regulating inflammation.

scholarly journals Transcription Factor Lbx1 Expression in Mouse Embryonic Stem Cell-Derived Phenotypes

2011 ◽  
Vol 2011 ◽  
pp. 1-7 ◽  
Author(s):  
Stefanie Schmitteckert ◽  
Cornelia Ziegler ◽  
Liane Kartes ◽  
Alexandra Rolletschek
Keyword(s):  
Transcription Factor ◽  
Developmental Stages ◽  
Troponin T ◽  
Es Cells ◽  
Expression Patterns ◽  
Embryonic Stem ◽  
Mouse Embryonic Stem Cell ◽  
Cardiac Cells ◽  
Cell Stage

Transcription factor Lbx1 is known to play a role in the migration of muscle progenitor cells in limb buds and also in neuronal determination processes. In addition, involvement of Lbx1 in cardiac neural crest-related cardiogenesis was postulated. Here, we used mouse embryonic stem (ES) cells which have the capacity to develop into cells of all three primary germ layers. Duringin vitrodifferentiation, ES cells recapitulate cellular developmental processes and gene expression patterns of early embryogenesis. Transcript analysis revealed a significant upregulation ofLbx1at the progenitor cell stage. Immunofluorescence staining confirmed the expression of Lbx1 in skeletal muscle cell progenitors and GABAergic neurons. To verify the presence of Lbx1 in cardiac cells, triple immunocytochemistry of ES cell-derived cardiomyocytes and a quantification assay were performed at different developmental stages. Colabeling of Lbx1 and cardiac specific markers troponin T, α-actinin, GATA4, and Nkx2.5 suggested a potential role in early myocardial development.

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