A pattern emerges in chromatin aging: AP-1 steals the show

During aging, transcriptional programs of cell identity are partially eroded, reducing cellular fitness and resilience. Patrick et al. 1 Patrick R. Naval-Sanchez M. Deshpande N. Huang Y. Zhang J. Chen X. Yang Y. Tiwari K. Esmaeili M. Tran M. et al. The activity of early-life gene regulatory elements is hijacked in aging through pervasive AP-1-linked chromatin opening. . 2024; 36: 1858-1881.e23https://doi.org/10.1016/j.cmet.2024.06.006 Google Scholar unveil a general mechanism for this process that consists of the progressive loss of transcription factor AP-1 from cell identity enhancers and its relocation by competition to stress-response elements. During aging, transcriptional programs of cell identity are partially eroded, reducing cellular fitness and resilience. Patrick et al. 1 Patrick R. Naval-Sanchez M. Deshpande N. Huang Y. Zhang J. Chen X. Yang Y. Tiwari K. Esmaeili M. Tran M. et al. The activity of early-life gene regulatory elements is hijacked in aging through pervasive AP-1-linked chromatin opening. . 2024; 36: 1858-1881.e23https://doi.org/10.1016/j.cmet.2024.06.006 Google Scholar unveil a general mechanism for this process that consists of the progressive loss of transcription factor AP-1 from cell identity enhancers and its relocation by competition to stress-response elements. The activity of early-life gene regulatory elements is hijacked in aging through pervasive AP-1-linked chromatin openingPatrick et al.Cell MetabolismJuly 2, 2024In BriefPatrick and Naval-Sanchez et al. offer a mechanistic connection between molecular remodeling in organismal maturation and aging. Through multi-omic analysis of both processes, they reveal a shared transcription factor binding pattern within genomic regulatory elements, underpinned by binding site abundance differences for AP-1, CTCF, and cell identity transcription factors. Full-Text PDF Open Access