Lineage Regulators Direct BMP and Wnt Pathways to Cell-Specific Programs during Differentiation and Regeneration
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Author(s)
Trompouki, Eirini
Bowman, Teresa V.
Lawton, Lee N.
Fan, Zi Peng
Wu, Dai-Chen
DiBiase, Anthony
Martin, Corey S.
Cech, Jennifer N.
Sessa, Anna K.
Leblanc, Jocelyn L.
Date Issued
October 2011
Journal
Cell
Publisher
Elsevier B.V.
Citation
Trompouki, Eirini, Teresa V. Bowman, Lee N. Lawton, Zi Peng Fan, Dai-Chen Wu, Anthony DiBiase, Corey S. Martin, et al. “Lineage Regulators Direct BMP and Wnt Pathways to Cell-Specific Programs During Differentiation and Regeneration.” Cell 147, no. 3 (October 2011): 577–589. © 2011 Elsevier Inc.
Version
Final published version
Abstract
BMP and Wnt signaling pathways control essential cellular responses through activation of the transcription factors SMAD (BMP) and TCF (Wnt). Here, we show that regeneration of hematopoietic lineages following acute injury depends on the activation of each of these signaling pathways to induce expression of key blood genes. Both SMAD1 and TCF7L2 co-occupy sites with master regulators adjacent to hematopoietic genes. In addition, both SMAD1 and TCF7L2 follow the binding of the predominant lineage regulator during differentiation from multipotent hematopoietic progenitor cells to erythroid cells. Furthermore, induction of the myeloid lineage regulator C/EBPα in erythroid cells shifts binding of SMAD1 to sites newly occupied by C/EBPα, whereas expression of the erythroid regulator GATA1 directs SMAD1 loss on nonerythroid targets. We conclude that the regenerative response mediated by BMP and Wnt signaling pathways is coupled with the lineage master regulators to control the gene programs defining cellular identity.
MIT Department
Massachusetts Institute of Technology. Computational and Systems Biology Program
Whitehead Institute for Biomedical Research
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Article is made available in accordance with the publisher's policy and may be subject to US copyright law. Please refer to the publisher's site for terms of use.
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DOI of Published Version
https://doi.org/10.1016/j.cell.2011.09.044
