ArticlePloS one2014
Mice carrying a hypomorphic Evi1 allele are embryonic viable but exhibit severe congenital heart defects.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 33 citations in OpenAlex.
- A cell atlas of the developing human outflow tract of the heart and its adult aortic valve derivatives.eLife · 2026Article
- PRDM3/16 regulate chromatin accessibility required for NKX2-1 mediated alveolar epithelial differentiation and function.Nature communications · 2024Article
- Genetics of Cardiac Aging Implicate Organ-Specific Variation.medRxiv : the preprint server for health sciences · 2024Article
- Molecular Pathways and Animal Models of Truncus Arteriosus.Advances in experimental medicine and biology · 2024Review
- Molecular Pathways and Animal Models of Semilunar Valve and Aortic Arch Anomalies.Advances in experimental medicine and biology · 2024Review
- PRDM3/16 Regulate Chromatin Accessibility Required for NKX2-1 Mediated Alveolar Epithelial Differentiation and Function.bioRxiv : the preprint server for biology · 2023Article
- EVI1-mediated Programming of Normal and Malignant Hematopoiesis.HemaSphere · 2023Review
- Mecom mutation related to radioulnar synostosis with amegakaryocytic thrombocytopenia reduces HSPCs in mice.Blood advances · 2023Article
- The Roles of Histone Lysine Methyltransferases in Heart Development and Disease.Journal of cardiovascular development and disease · 2023Review
- Epigenetic landscape reveals MECOM as an endothelial lineage regulator.Nature communications · 2023Article
- EVI1 expression in early-stage breast cancer patients treated with neoadjuvant chemotherapy.BMC cancer · 2022Article
- SOX9 in organogenesis: shared and unique transcriptional functions.Cellular and molecular life sciences : CMLS · 2022Review
- MECOM-associated syndrome: a heterogeneous inherited bone marrow failure syndrome with amegakaryocytic thrombocytopenia.Blood advances · 2018Article
- Detection of QTL for traits related to adaptation to sub-optimal climatic conditions in chickens.Genetics, selection, evolution : GSE · 2017Article
- Targeted Sequencing of Lung Function Loci in Chronic Obstructive Pulmonary Disease Cases and Controls.PloS one · 2017Article
- Evi1 regulates Notch activation to induce zebrafish hematopoietic stem cell emergence.The EMBO journal · 2016Article
- Functional features of EVI1 and EVI1Δ324 isoforms of MECOM gene in genome-wide transcription regulation and oncogenicity.Oncogene · 2016Article
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Authors and funding
17 authors at 7 institutions in 5 countries.
Funding
Abstract
The ecotropic viral integration site 1 (Evi1) oncogenic transcription factor is one of a number of alternative transcripts encoded by the Mds1 and Evi1 complex locus (Mecom). Overexpression of Evi1 has been observed in a number of myeloid disorders and is associated with poor patient survival. It is also amplified and/or overexpressed in many epithelial cancers including nasopharyngeal carcinoma, ovarian carcinoma, ependymomas, and lung and colorectal cancers. Two murine knockout models have also demonstrated Evi1's critical role in the maintenance of hematopoietic stem cell renewal with its absence resulting in the death of mutant embryos due to hematopoietic failure. Here we characterize a novel mouse model (designated Evi1(fl3)) in which Evi1 exon 3, which carries the ATG start, is flanked by loxP sites. Unexpectedly, we found that germline deletion of exon3 produces a hypomorphic allele due to the use of an alternative ATG start site located in exon 4, resulting in a minor Evi1 N-terminal truncation and a block in expression of the Mds1-Evi1 fusion transcript. Evi1(δex3/δex3) mutant embryos showed only a mild non-lethal hematopoietic phenotype and bone marrow failure was only observed in adult Vav-iCre/+, Evi1(fl3/fl3) mice in which exon 3 was specifically deleted in the hematopoietic system. Evi1(δex3/δex3) knockout pups are born in normal numbers but die during the perinatal period from congenital heart defects. Database searches identified 143 genes with similar mutant heart phenotypes as those observed in Evi1(δex3/δex3) mutant pups. Interestingly, 42 of these congenital heart defect genes contain known Evi1-binding sites, and expression of 18 of these genes are also effected by Evi1 siRNA knockdown. These results show a potential functional involvement of Evi1 target genes in heart development and indicate that Evi1 is part of a transcriptional program that regulates cardiac development in addition to the development of blood.
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