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Etv inactivation effect on embryonic lung development

ABSTRACT: ETV4 and ETV5 are FGF-activated transcription factor genes. Inactivation of Etv4 and Etv5 in the lung epithelium led to prolonged branch tip growth and delayed new branch formation. We used microarrays to detail the global programme of gene expression in embryonic day 13.5 mouse lungs and identified distinct classes of dysregulated genes affect by Etv4;5 epithelial specific knockout.

ORGANISM(S): Mus musculus

PROVIDER: GSE80734 | GEO | 2016/04/28

SECONDARY ACCESSION(S): PRJNA319836

REPOSITORIES: GEO

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RNASeq to investigate ETV4 and ETV5 function in human foetal lung tip progenitor cells

Project description:In order to understand transcription factor ETV4 and ETV5 function, we have knocked down ETV4 and ETV5 synergistically in human foetal lung tip progenitor organoids using an inducible CRISPRi system. We discovered that ETV double knockdown led to organoid cell self-renewal defects

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E3 ubiquitin ligase Rfwd2 inactivation effect on embryonic lung development

Project description:Transcriptome analysis by RNA-seq of lungs from control and Rfwd2 epithelial-specific conditional knockout mice at embryonic 13.5 day age. RFWD2, is an E3 ubiquitin ligase that modifies specific target proteins, priming their degradation via the ubiquitin proteasome system. Rfwd2 deficiency led to a striking halt in branching morphogenesis shortly after secondary branch formation. In the mutant lung, two ETS transcript factors essential for normal lung branching, ETV4 and ETV5, were upregulated at the protein, but not transcript level. Introduction of Etv loss-of-function alleles into the Rfwd2 mutant background attenuated the branching phenotype, suggesting that RFWD2 functions at least in part through degrading ETV proteins. As a number of E3 ligases are known to target factors important for lung development, our findings provides a preview of a protein-level regulatory network essential for lung branching morphogenesis.

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Transcription profiling of mouse knockouts for Etv4 and Etv5 - plusGDNF and minusGDNF comparison using U74Av2 and 430A arrays

Project description:GDNF signaling through the Ret receptor tyrosine kinase is critical for ureteric bud branching morphogenesis during kidney development yet few of the downstream genes are currently known. We find that the ETS transcription factors Etv4 and Etv5 are positively regulated by Ret signaling in ureteric bud tips. Etv4-/-Etv5+/- mice display either renal agenesis or severe hypodysplasia, while kidney development fails completely in double homozygotes. We identify several genes whose expression in the ureteric bud depends on Etv4 and Etv5, including Cxcr4, Myb, Met, Mmp14. Thus, Etv4 and Etv5 are key components of a gene network downstream of Ret that promotes and controls renal branching morphogenesis. Experiment Overall Design: 3 plus GDNF and 2 minus GDNF chips were analyzed with different pooled samples for each chip (U74Av2 and 430A). Sample comparisons and statistical analysis were performed using dChip 1.3, using the Comparison Analysis feature to identify genes differentially expressed between the two groups. The following filtering criteria were used: the “lower limit” for fold-change between the means of the +GDNF and -GDNF samples must exceed 1.2 with a 90% confidence limit, and the absolute difference between the two group means must exceed 100.

2009-10-02 | E-GEOD-18267 | biostudies-arrayexpress

Spatiotemporal lineage derepression by cell crowding-induced ETV4 inactivation

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