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Abstract Senescent cells accumulate in aging tissues and secrete a complex array of bioactive factors that alter the surrounding environment. While transient signaling can support tissue repair, persistent activity drives chronic low-grade inflammation and contributes to age-related diseases. These factors can spread damage to nearby cells and disrupt immune balance, creating a self-reinforcing cycle.
Abstract The growth of telomerase-deficient cancers depends on the alternative lengthening of telomeres (ALT), a homology-directed telomere-maintenance pathway. ALT telomeres exhibit a unique chromatin environment and generally lack the nucleosome remodeler ATRX, pointing to an epigenetic basis for ALT. Recently, we identified a protective role for the ATRX-interacting macroH2A1.2 histone variant during homologous recombination and replication stress (RS).
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