Differential regulation of cranial and cardiac neural crest by Serum Response Factor
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA776000 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR16612703_1.fastq.gz | Fastqsanger.gz | |||
| SRR16612703_2.fastq.gz | Fastqsanger.gz | |||
| SRR16612704_1.fastq.gz | Fastqsanger.gz | |||
| SRR16612704_2.fastq.gz | Fastqsanger.gz | |||
| SRR16612705_1.fastq.gz | Fastqsanger.gz |
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Project description:The goal of this experiment was to identify genes regulated by Serum Response Factor (SRF) in the neural crest in the craniofacial region, including whether there were different targets in different craniofacial prominences. SRF is an essential transcription factor that influences many cellular processes including cell proliferation, migration, and differentiation. SRF directly regulates and is required for immediate early gene (IEG) and actin cytoskeleton-related gene expression. SRF coordinates these competing transcription programs through discrete sets of cofactors, the Ternary Complex Factors (TCFs) and Myocardin Related Transcription Factors (MRTFs). The relative contribution of these two programs to in vivo SRF activity and mutant phenotypes is not fully understood. To study how SRF utilizes its cofactors during development, we generated a knock-in SrfaI allele in mice harboring point mutations that disrupt SRF-MRTF-DNA complex formation but leave SRF-TCF activity unaffected. Homozygous SrfaI/aI mutants die at E10.5 with notable cardiovascular phenotypes, and neural crest conditional mutants succumb at birth to defects of the cardiac outflow tract but display none of the craniofacial phenotypes associated with complete loss of SRF in that lineage.
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Project description:The cranial neural crest cells are pluripotent cells that provide head skeletogenic mesenchyme and are crucial for craniofacial patterning. Here, we analyzed the in vivo chromatin landscapes of mouse cranial neural crest subpopulations. Early postmigratory neural crest subpopulations contributing to distinct mouse craniofacial structures displayed similar chromatin accessibility patterns, yet differed transcriptionally. Accessible promoters and enhancers of differentially silenced genes carried H3K27me3/H3K4me2 bivalent chromatin marks embedded in large Ezh2-dependent Polycomb domains, indicating transcriptional poising. These postmigratory bivalent regions were already present in neural crest premigratory progenitors. At Polycomb domains, H3K27me3 antagonized H3K4me2 deposition, which was restricted to accessible sites. Thus, bivalent Polycomb domains provide a chromatin template for the regulation of cranial neural crest cell positional identity in vivo contributing novel insights into the epigenetic regulation of face morphogenesis.
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