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Diet-induced chromatin states influence intestinal stem cell memory

Saiz, D. R.; Barrera Millan, Y.; Hartley McDermott, T.; Cerna, G.; Sankar, S.; Farnsworth, F.; Uher, E.; Lahiri, G.; Lintecum, K.; Mullen, K.; Bartelle, B. B.; Mana, M. D.

2026-02-20 cell biology
10.64898/2026.02.19.706894 bioRxiv
Show abstract

Intestinal stem cells (ISCs) integrate dietary cues through a metabolic-transcriptional axis, but whether these mechanisms create a lasting epigenetic memory remains unclear. Here, we investigate diet-induced chromatin adaptations in ISCs using a high-fat Western diet (HFD) mouse model. HFD broadly remodels chromatin accessibility, altering pre-existing open regulatory regions. Many differentially accessible regions (DARs) persist during the differentiation of ISCs into transient amplifying cells (TACs). Notably, HFD-induced DARs are retained following diet normalization despite phenotypic reversibility, and HFD re-exposure enhances ISC self-renewal and adenoma growth compared with naive HFD exposure. The HFD-induced chromatin changes require Ppar-d/a nuclear receptors but are independent of their transcriptional targets. Although a subset of HFD-induced DARs is maintained following Apc loss, extensive chromatin remodeling driven by tumor suppressor inactivation largely overrides diet-dependent differences in Lgr5 ISCs. Together, these findings demonstrate that ISCs retain a chromatin-based memory of dietary fat exposure.

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