ArticleBMC developmental biology2009
A tamoxifen inducible knock-in allele for investigation of E2A function.
Article in BMC developmental biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- Depletion of ID3 enhances mesenchymal stem cells therapy by targeting BMP4 in Sjögren's syndrome.Cell death & disease · 2020Article
- Reversible modulation of SIRT1 activity in a mouse strain.PloS one · 2017Article
- Modeling Murine Gastric Metaplasia Through Tamoxifen-Induced Acute Parietal Cell Loss.Methods in molecular biology (Clifton, N.J.) · 2016Article
- The estrogen receptor fusion system in mouse models: a reversible switch.Cold Spring Harbor protocols · 2015Article
- Dynamic changes in E-protein activity regulate T reg cell development.The Journal of experimental medicine · 2014Article
- Genes that confer the identity of the renin cell.Journal of the American Society of Nephrology : JASN · 2011Article
- Stage-specific functions of E-proteins at the β-selection and T-cell receptor checkpoints during thymocyte development.Immunologic research · 2011Article
- Control of the differentiation of regulatory T cells and T(H)17 cells by the DNA-binding inhibitor Id3.Nature immunology · 2011Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundE-proteins are transcription factors important for the development of a variety of cell types, including neural, muscle and lymphocytes of the immune system. E2A, the best characterized E-protein family member in mammals, has been shown to have stage specific roles in cell differentiation, lineage commitment, proliferation, and survival. However, due to the complexity of E2A function, it is often difficult to separate these roles using conventional genetic approaches. Here, we have developed a new genetic model for reversible control of E2A protein activity at physiological levels. This system was created by inserting a tamoxifen-responsive region of the estrogen receptor (ER) at the carboxyl end of the tcfe2a gene to generate E2AER fusion proteins. We have characterized and analyzed the efficiency and kinetics of this inducible E2AER system in the context of B cell development.
resultsB cell development has been shown previously to be blocked at an early stage in E2A deficient animals. Our E2AER/ER mice demonstrated this predicted block in B cell development, and E2AER DNA binding activity was not detected in the absence of ligand. In vitro studies verified rapid induction of E2AER DNA binding activity upon tamoxifen treatment. While tamoxifen treatment of E2AER/ER mice showed inefficient rescue of B cell development in live animals, direct exposure of bone marrow cells to tamoxifen in an ex vivo culture was sufficient to rescue and support early B cell development from the pre-proB cell stage.
conclusionThe E2AER system provides inducible and reversible regulation of E2A function at the protein level. Many previous studies have utilized over-expression systems to induce E2A function, which are complicated by the toxicity often resulting from high levels of E2A. The E2AER model instead restores E2A activity at an endogenous level and in addition, allows for tight regulation of the timing of induction. These features make our E2AER ex vivo culture system attractive to study both immediate and gradual downstream E2A-mediated events.
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