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Biology subjects

LE COZ, M.

Publications and source records attributed to LE COZ, M..

2 recordsLinked to original sources

BRN2 preserves the melanocyte lineage following ionizing radiation

Adult stem cells maintain tissue homeostasis, but mechanisms preserving their integrity under stress remain incompletely understood. Here, we identify BRN2 (POU3F2), previously implicated in neuronal development, reprogramming of fibroblasts to neurons and in melanoma proliferation, migration and DNA-damage responses, as a key guardian of melanocyte stem cells. Remarkably, we reveal that while Brn2-deficient mice maintain their McSC compartment and normal pigmentation for up to 95 weeks, in contrast, rapid, dose-dependent, permanent hair depigmentation associated with the disappearance of detectable McSCs and differentiated melanocytes occurs in Brn2 KO mice exposed to ionizing radiation but not in WT mice. Importantly, our results indicate that in human follicular melanocytes BRN2 activity in melanocyte stem cells (McSCs) declines with age and that Brn2 promotes melanocyte stem cell regeneration by restraining stress-induced melanocytic differentiation. Our findings establish a previously unrecognized in vivo requirement for BRN2 in preserving the integrity of the melanocyte lineage following ionizing radiation, revealing a stress-dependent function distinct from its largely dispensable role in steady-state McSC maintenance.

cell biology↗

BRN2 suppresses stress-induced hair greying

Adult stem cells maintain tissue homeostasis and regenerative capacity, but mechanisms preserving their integrity under stress remain incompletely understood. Here, we identify BRN2 (POU3F2), a POU-domain transcription factor, as a regulator of melanocyte lineage homeostasis and response to genotoxic stress. Single-cell transcriptomic analyses identified Brn2 among transcription factors preferentially active in melanocyte stem cells (McSCs), with BRN2 activity declining with age in human hair follicle melanocytic cells. Melanocyte-specific Brn2 deletion increased melanocyte differentiation and accumulation in the hair bulb, while downregulating DNA-repair and chromosome-maintenance programs. Despite these changes, Brn2 loss caused neither spontaneous hair greying nor detectable McSC depletion under steady-state conditions. Following ionizing radiation, however, Brn2-deficient cells showed altered DNA-damage responses, reduced mitotic signatures, increased p53 and p21, and enhanced melanocytic differentiation. Irradiated Brn2-deficient mice developed rapid, dose-dependent, permanent hair depigmentation associated with McSC and melanocyte depletion. Thus, BRN2 links POU-dependent transcriptional control to stem-cell resilience under genotoxic stress, preserving melanocyte regenerative capacity and protecting against irradiation-induced hair greying.

cell biology↗