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Sf3b4 mutation in Xenopus tropicalis causes RNA splicing defects and gene dysregulation across development and disrupts cranial neural crest cell migration and survival

ABSTRACT: Sf3b4 mutation in Xenopus tropicalis causes RNA splicing defects and gene dysregulation across development and disrupts cranial neural crest cell migration and survival

PROVIDER: PRJNA1047118 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27008135_1.fastq.gz	Fastqsanger.gz
	SRR27008135_2.fastq.gz	Fastqsanger.gz
	SRR27008136_1.fastq.gz	Fastqsanger.gz
	SRR27008136_2.fastq.gz	Fastqsanger.gz
	SRR27008137_1.fastq.gz	Fastqsanger.gz

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Sf3b4 mutation in Xenopus tropicalis causes RNA splicing defects and gene dysregulation across development and disrupts cranial neural crest cell migration and survival

Project description:Nager syndrome is a rare craniofacial and limb disorder characterized by midface retrusion, micrognathia, absent thumbs, and radial hypoplasia. This disorder results from haploinsufficiency of SF3B4 (splicing factor 3b, subunit 4) a component of the pre-mRNA spliceosomal machinery. The spliceosome is a complex of RNA and proteins that function together to remove introns and join exons from transcribed pre-mRNA. While the spliceosome is present and functions in all cells of the body, most spliceosomopathies – including Nager syndrome – are cell/tissue-specific in their pathology. In Nager syndrome patients, it is the neural crest (NC)-derived craniofacial skeletal structures that are primarily affected. To understand the pathomechanism underlying this condition, we generated a Xenopus tropicalis sf3b4 mutant line using the CRISPR/Cas9 gene editing technology. Here we describe the sf3b4 mutant phenotype at neurula, tail bud, and tadpole stages, and performed temporal RNA-sequencing analysis to characterize the splicing events and transcriptional changes underlying this phenotype. Our data show that while loss of one copy of sf3b4 is largely inconsequential in Xenopus tropicalis, homozygous deletion of sf3b4 causes major splicing defects and gene dysregulation, which disrupt cranial NC cell migration and survival, thereby pointing at an essential role of Sf3b4 in craniofacial development.

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Post-transcriptional regulation in cranial neural crest cells expands developmental potential [I]

Project description:Developmental potential is progressively restricted after germ layer specification during gastrulation. However, cranial neural crest cells challenge this paradigm, as they develop from anterior ectoderm yet give rise to both mesodermal derivatives of the craniofacial skeleton and ectodermal derivatives of the peripheral nervous system. How cranial neural crest cells differentiate into multiple lineages is poorly understood. Here, we demonstrate that cranial neural crest cells possess a transient state of increased chromatin accessibility; and that the earliest premigratory neural crest are biased towards either a neuronal or ectomesenchymal fate, with each lineage expressing distinct factors from the pluripotent state. We profile the spatiotemporal emergence of each neural crest population and demonstrate that the ectomesenchymal lineage forms prior to the neuronal progenitors. Expression of the pluripotency microRNA family miR-302 is maintained in cranial neural crest cells and genetic deletion leads to precocious specification of the ectomesenchymal lineage. We find that miR-302 directly targets Sox9 to slow the timing of ectomesenchyme induction and regulates multiple genes involved in chromatin condensation to maintain accessibility for neuronal differentiation. Loss of mir-302 results in reduced chromatin accessibility in the neuronal progenitor lineage of neural crest and a reduction in peripheral neuron differentiation. Our findings reveal a post-transcriptional mechanism governed by miRNAs from pluripotency as an important mechanism to expand developmental potential of cranial neural crest.

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Post-transcriptional regulation in cranial neural crest cells expands developmental potential [II]

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