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Reactivation of an Embryonic Cardiac Neural Crest Transcriptional Subcircuit During Zebrafish Heart Regeneration [bulk RNA-seq]

ABSTRACT: During vertebrate development, the heart primarily arises from mesoderm, with crucial contributions from cardiac neural crest cells that migrate to the heart and form a variety of cardiovascular derivatives. Here, by integrating bulk and single cell RNAseq with ATAC-seq, we identify a gene regulatory subcircuit specific to migratory cardiac crest cells composed of key transcription factors egr1, sox9a, tfap2a and ets1. Notably, we show that cells expressing the canonical neural crest gene sox10 are essential for proper cardiac regeneration in adult zebrafish. Furthermore, expression of all transcription factors from the migratory cardiac crest gene subcircuit are reactivated after injury at the wound edge. Together, our results uncover a developmental gene regulatory network that is important for cardiac neural crest fate determination, with key factors re-activated during regeneration.

ORGANISM(S): Danio rerio

PROVIDER: GSE287815 | GEO | 2025/01/30

REPOSITORIES: GEO

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	GSE287815_17CNCvs24hTNC_onepage.txt.gz	Txt
	GSE287815_20ss_CNC_3reps_counts.txt.gz	Txt

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Reactivation of an Embryonic Cardiac Neural Crest Transcriptional Subcircuit During Zebrafish Heart Regeneration [bulk ATAC-seq]

Project description:During vertebrate development, the heart primarily arises from mesoderm, with crucial contributions from cardiac neural crest cells that migrate to the heart and form a variety of cardiovascular derivatives. Here, by integrating bulk and single cell RNAseq with ATAC-seq, we identify a gene regulatory subcircuit specific to migratory cardiac crest cells composed of key transcription factors egr1, sox9a, tfap2a and ets1. Notably, we show that cells expressing the canonical neural crest gene sox10 are essential for proper cardiac regeneration in adult zebrafish. Furthermore, expression of all transcription factors from the migratory cardiac crest gene subcircuit are reactivated after injury at the wound edge. Together, our results uncover a developmental gene regulatory network that is important for cardiac neural crest fate determination, with key factors re-activated during regeneration.

2025-01-30 | GSE287813 | GEO

Reactivation of an Embryonic Cardiac Neural Crest Transcriptional Subcircuit During Zebrafish Heart Regeneration [scRNA-seq]

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TFAP2 paralogs regulate midfacial development in part through a conserved ALX genetic pathway [RNA-Seq]

Project description:Cranial neural crest development is governed by positional gene regulatory networks (GRNs). Fine-tuning of the GRN components underly facial shape variation, yet how those in the midface are connected and activated remain poorly understood. Here, we show that concerted inactivation of Tfap2a and Tfap2b in the murine neural crest, even during the late migratory phase, results in a midfacial cleft and skeletal abnormalities. Bulk and single-cell RNA-seq profiling reveal that loss of both Tfap2 members dysregulates numerous midface GRN components involved in midface morphogenesis, patterning, and differentiation. Notably, Alx1/3/4 (Alx) transcript levels are reduced, while ChIP-seq analyses suggest TFAP2 directly and positively regulates Alx gene expression. TFAP2 and ALX co-expression in midfacial neural crest cells of both mouse and zebrafish further implies conservation of this regulatory axis across vertebrates. Consistent with this notion in zebrafish, tfap2a mutants present abnormal alx3 expression patterns, Tfap2a binds alx loci, and tfap2a-alx3 genetic interactions are observed. Together, these data demonstrate TFAP2 paralogs regulate vertebrate midfacial development by activating expression of ALX transcription factors.

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TFAP2 paralogs regulate midfacial development in part through a conserved ALX genetic pathway [scRNA-seq]

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TFAP2 paralogs regulate midfacial development in part through a conserved ALX genetic pathway [ChIP-seq]

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Ankrd11, a chromatin regulator and a KBG syndrome risk gene, is a critical regulator of cardiac neural crest cell biology and heart development [MERSCOPE]

Project description:ANKRD11 (Ankyrin Repeat Domain 11) is a chromatin regulator and a risk gene for KBG syndrome, a rare developmental disorder characterized by multiple organ abnormalities, including cardiac defects. However, the role of ANKRD11 in heart development is unknown. The neural crest plays a leading role in embryonic heart development, and its dysfunction is implicated in congenital heart defects. We demonstrate conditional knockout of Ankrd11 in the murine embryonic neural crest results in persistent truncus arteriosus, ventricular dilation, and impaired ventricular contractility. We further show these defects occur due to aberrant cardiac neural crest cell organization leading to outflow tract septation failure. Finally, knockout of Ankrd11 in the neural crest leads to impaired expression of various transcription factors, chromatin remodelers and signaling pathways, including mTOR, BMP and TGF-β in the cardiac neural crest cells. In this work, we identify Ankrd11 as a novel regulator of neural crest-mediated heart development and function.

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Project description:The complex interplay between signaling systems, transcription factors, and cis-regulatory elements required for development are encoded within gene regulatory networks (GRN). Although GRNs have greatly expanded our understanding of cell fate decisions during embryogenesis, they are typically assembled via a candidate-based approach, which fails to consider the tissue specific functions more broadly expressed TFs may employ. To address this, we combined a TF-focused CRISPR screen with epigenomic and transcriptional profiling of human neural crest cells. This approach unbiasedly identified several key regulators of human neural crest cell development, including the ubiquitous AP-1 transcription factor complex. Functional characterization of AP-1 demonstrated it is a major regulator of neural crest identity, working with the cell type specific TF, TFAP2A, to shape the neural crest epigenome. Interestingly, overexpression of AP-1 and TFAP2A in human embryonic stem cells is sufficient to drive neural crest identity, suggesting a critical role for AP-1 in the transition from pluripotency to more specialized stem cell states. Furthermore, we demonstrate that AP-1 serves as a nuclear effector of FGF/MAPK signaling in human neural crest cells, a previously missing link between FGF signaling and neural crest development. Our results demonstrate signaling effectors carry out cell-type specific enhancer selection and may contribute to our efforts in engineering neural crest cells for the purpose of tissue repair and regeneration.

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CUT&RUN profiling of Tfap2a binding genome-wide using zebrafish embryos at 24hpf

Project description:The purpose of this study was to identify Tfap2a binding genome-wide in zebrafish embryos at 24hpf. Tfap2 transcription factors are essential regulators of neural crest development, melanocyte differentiation, and melanoma progression. We aimed to identify Tfap2a-occupied genes to determine direct Tfap2a-regulated transcriptional networks.

2023-12-18 | GSE250450 | GEO

Heterodimerization of Tfap2 pioneer factors drives epigenomic remodeling during neural crest specification

Project description:Cell fate commitment is a stepwise process, in which multipotent progenitors transition through sequential regulatory states as they become fate restricted. Recent studies have highlighted the extensive transcriptomic shifts that typify cell differentiation, but our understanding of the epigenetic mechanisms underlying these changes is still superficial. To examine how chromatin states are reorganized during cell fate commitment in an in vivo system, we examined the function of pioneer factor Tfap2a at discrete stages of neural crest development. Our results show that TFAP2a activates distinct sets of genomic regions during induction and specification of neural crest cells. Genomic occupancy analysis revealed that the repertoire of TFAP2a targets depends upon its dimerization with paralogous proteins TFAP2c and TFAP2b. During gastrula stages, TFAP2a/c heterodimers activate components of the neural plate border induction program. As neurulation begins, TFAP2a trades partners, and TFAP2a/b heterodimers reorganize the epigenomic landscape of progenitor cells to promote neural crest specification. We propose that this molecular switch acts to drive progressive cell commitment, remodeling the epigenomic landscape to define the presumptive neural crest. Our findings show how pioneer factors regulate distinct genomic targets in a stage-specific manner, and highlight how paralogy can serve as an evolutionary strategy to diversify the function of the regulators that control embryonic development.

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