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VRTN Regulates the Number of Thoracic Vertebrae During Vertebrate Development

ABSTRACT: VRTN Regulates the Number of Thoracic Vertebrae During Vertebrate Development

PROVIDER: PRJNA347516 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR4407930.fastq.gz	Fastqsanger.gz
	SRR4407924.fastq.gz	Fastqsanger.gz
	SRR4407925.fastq.gz	Fastqsanger.gz
	SRR4407926.fastq.gz	Fastqsanger.gz
	SRR4407927.fastq.gz	Fastqsanger.gz

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VRTN Regulates the Number of Thoracic Vertebrae During Vertebrate Development [RNA-seq]

Project description:The number of vertebrae is precisely defined in almost all vertebrate species, but varies considerably in pigs, making this animal an excellent model for studying the mechanisms that control vertebral number. Vertnin (VRTN) variants have been associated with thoracic vertebral number (TVN) in pigs. However, the causal relation between VRTN and TVN remains to be established, and the role of VRTN in modulating TVN is not yet known. Here, we demonstrate that VRTN is one of the genes responsible for determining TVN. We show that VRTN is a DNA-binding transcription factor, which is essential for the formation of thoracic vertebrae during early embryogenesis as VRTN-null mice showed embryonic lethality at the later thoracic somite stages and had fewer somites than their wild-type and heterozygous littermates. We also show that VRTN causative variants increase Notch signaling in pig embryos, suggesting that VRTN controls segment number by altering the pace of somatic segmentation. These findings advance our understanding of the role of VRTN in the formation of thoracic vertebrae and reveal new aspects of somite developmental biology.

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VRTN Regulates the Number of Thoracic Vertebrae During Vertebrate Development [ChIP-seq]

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VRTN Regulates the Number of Thoracic Vertebrae During Vertebrate Development

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Project description:Intratumor mutational heterogeneity has been documented in primary non-small cell lung cancer. Here, we elucidate mechanisms of tumor evolution and heterogeneity in metastatic thoracic tumors (lung adenocarcinoma and thymic carcinoma) using whole-exome and transcriptome sequencing, SNP array for copy number alterations (CNA) and mass spectrometry-based quantitative proteomics of metastases obtained by rapid autopsy. APOBEC-mutagenesis, promoted by increased expression of APOBEC3 region transcripts and associated with a high-risk germline APOBEC3 variant, strongly correlated with mutational tumor heterogeneity. TP53 mutation status was associated with APOBEC hypermutator status. Interferon pathways were enriched in tumors with high APOBEC mutagenesis and IFN- induced expression of APOBEC3B in lung adenocarcinoma cells in culture suggesting a role for the immune microenvironment in the generation of mutational heterogeneity. CNA occurring late in tumor evolution correlated with downstream transcriptomic and proteomic heterogeneity, although global proteomic heterogeneity was significantly greater than transcriptomic and CNA heterogeneity. These results illustrate key mechanisms underlying multi-dimensional heterogeneity in metastatic thoracic tumors.

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