Linker histone regulates the myeloid versus lymphoid bifurcation of multipotent hematopoietic stem and progenitors.

Kutay Karatepe, Bruna Mafra de Faria, Jian Zhang, Xinyue Chen, Hugo Pinto, Dmitry Fyodorov, Esen Sefik, Michael A Willcockson, Richard A Flavell, Arthur I Skoultchi, Shangqin Guo

Department of Cell Biology, Yale University, New Haven, CT 06520.Department of Cell Biology, Yale University, New Haven, CT 06520. · pubmed

Paper

Abstract

Myeloid-biased differentiation of multipotent hematopoietic stem and progenitor cells (HSPCs) occurs with aging or exhaustion. The molecular mechanism(s) responsible for this fate bias remain unclear. Here, we report that linker histone regulates HSPC fate choice at the lymphoid versus myeloid bifurcation. Linker histones package nucleosomes and compact chromatin. HSPCs expressing a doxycycline (dox)-inducible H1.0 transgene favor the lymphoid fate, display strengthened nucleosome organization, and reduced chromatin accessibility at subsets of genomic regions. The genomic regions showing reduced chromatin accessibility host many known marker genes of myeloid-biased HSCs. The transcription factor

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Research summary

The paper claims that linker histone regulates the fate choice of hematopoietic stem and progenitor cells towards lymphoid or myeloid lineages. This research is relevant as it explores the molecular mechanisms underlying age-related changes in stem cell differentiation, which could contribute to understanding the aging process and potential interventions.

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