Loss of linker histone H1 in cellular senescence.
作者： Ryo Funayama , Motoki Saito , Hiroko Tanobe , Fuyuki Ishikawa
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摘要: Cellular senescence is a tumor-suppressing mechanism that accompanied by characteristic chromatin condensation called senescence-associated heterochromatic foci (SAHFs). We found individual SAHFs originate from chromosomes. do not show alterations of posttranslational modifications core histones mark condensed in mitotic chromosomes, apoptotic chromatin, or transcriptionally inactive heterochromatin. Remarkably, SAHF-positive senescent cells lose linker histone H1 and exhibit increased levels chromatin-bound high mobility group A2 (HMGA2). The expression N-terminally enhanced green fluorescent protein (EGFP)–tagged induces premature phenotypes, including phosphorylated p53, p21, hypophosphorylated Rb, decrease the endogenous level but p16 accumulation SAHF formation. However, simultaneous ectopic hemagglutinin-tagged HMGA2 EGFP-tagged leads to significant formation (P < 0.001). It known HMG proteins compete for common binding site, DNA. These results suggest are novel type involving DNA–binding proteins.
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