Vitamin B12 is a limiting factor for induced cellular plasticity and tissue repair
Kovatcheva M, Melendez E, Chondronasiou D, Pietrocola F, Bernad R, Caballe A, Junza A, Capellades J, Holguín-Horcajo A, Prats N, Durand S, Rovira M, Yanes O, Attolini C, Kroemer G, Serrano M (2023) Nature Metabolism Nov 16 doi: 10.1038/s42255-023-00916-6
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Abstract:
Transient reprogramming by the expression of OCT4, SOX2, KLF4 and MYC (OSKM) is a therapeutic strategy for tissue regeneration and rejuvenation, but little is known about its metabolic requirements. Here we show that OSKM reprogramming in mice causes a global depletion of vitamin B12 and molecular hallmarks of methionine starvation. Supplementation with vitamin B12 increases the efficiency of reprogramming both in mice and in cultured cells, the latter indicating a cell-intrinsic effect. We show that the epigenetic mark H3K36me3, which prevents illegitimate initiation of transcription outside promoters (cryptic transcription), is sensitive to vitamin B12 levels, providing evidence for a link between B12 levels, H3K36 methylation, transcriptional fidelity and efficient reprogramming. Vitamin B12 supplementation also accelerates tissue repair in a model of ulcerative colitis. We conclude that vitamin B12, through its key role in one-carbon metabolism and epigenetic dynamics, improves the efficiency of in vivo reprogramming and tissue repair.FAB RESEARCH COMMENT:
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