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Preprint Links Blood Cell Aging to Loss of Regulatory Coherence On June 4, Harlan Stevens’ team posted a preprint analyzing 385,509 paired single‑cell profiles from 77 healthy donors aged 17–81. For each cell they measured gene expression and chromatin accessibility. In hematopoietic stem and early progenitor cells, stress and myeloid programs increase with age while self‑renewal and lymphoid programs decline. The researchers sought a common pattern linking these shifts. By comparing the same cell type across ages, they separated intracellular changes from shifts in cell‑type proportions. Using gene activity and accessibility data they computationally reconstructed regulatory programs: a regulator linked to DNA regions and the genes it presumably controls. They defined “regulatory entropy” as several coordinated observations: gene‑activity variability rises within a cell type, the link between open DNA and its target gene weakens, open regions lose sharp boundaries, and the number of regulator proteins in donor‑specific networks declines with age. Programs whose regulatory sites lie close to their genes tend to be preserved or strengthened, whereas identity programs that depend on distal enhancers more often weaken. The same trend appears when comparing regulators with similar roles in hematopoiesis. The authors hypothesize that stress response, myeloid skewing, and loss of cellular identity may be linked manifestations of regulatory‑network instability. They suggest that the architecture of a gene program could predict how much it will weaken with age within a hematopoietic lineage. 🔗 Read original →