Integration of cell cycle control and cell fate choice in M-CSF-instructed myeloid lineage commitment of hematopoietic stem cells

Abstract

We have shown recently that under hematopoietic stress conditions of infection high systemic levels of M-CSF can directly instruct myeloid gene expression and differentiation preference of HSC by activation of the myeloid master regulator PU.1 (Mossadegh-Keller et al, Nature, 2013), demonstrating that stem cells are direct targets of lineage instruction by cytokines. Moreover, we have shown earlier that HSC deficient for the transcription factor MafB are more sensible to M-CSF induced PU.1 activation and myeloid lineage commitment (Sarrazin et al, Cell, 2009).