Journal article
Regulation of lymphoid versus myeloid fate 'choice' by the transcription factor Mef2c
S Stehling-Sun, J Dade, SL Nutt, RP DeKoter, FD Camargo
Nature Immunology | Published : 2009
DOI: 10.1038/ni.1694
Abstract
Despite advances in the identification of lymphoid-restricted progenitor cells, the transcription factors essential for their generation remain to be identified. Here we describe an unexpected function for the myeloid oncogene product Mef2c in lymphoid development. Mef2c deficiency was associated with profound defects in the production of B cells, T cells, natural killer cells and common lymphoid progenitor cells and an enhanced myeloid output. In multipotent progenitors, Mef2c was required for the proper expression of several key lymphoid regulators and restriction of the myeloid fate. Our studies also show that Mef2c was a critical transcriptional target of the transcription factor PU.1 du..
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Awarded by National Institutes of Health
Funding Acknowledgements
We thank J. Schwartz (Albany Medical College) and Brian Black (University of California, San Francisco) for mutant mice; G. Bell and P. Thiru for microarray data analysis; members of the Jaenisch laboratory for discussions; R. Jimenez for mouse handling and technical support; and L. Lawton (Whitehead Institute for Biomedical Research) for reagents. Supported by the Whitehead Institute Fellows (F. D. C.) and the National Institutes of Health (AI052175 to R. P. D.).