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Selenium‐induced senescence involves heterochromatin formation
Author(s) -
Rouse Jallah J,
Cheng Wen-Hsing
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.1022.1
Subject(s) - heterochromatin , senescence , telomere , microbiology and biotechnology , biology , ataxia telangiectasia , histone h3 , histone , chemistry , dna damage , chromatin , genetics , dna
Selenium can induce a senescence response in a manner depending on ataxia‐telangiectasia mutated (ATM) and reactive oxygen species (ROS). During cellular senescence, induction of heterochromatin is known to suppress the transcription of genes in association with proliferation. Although senescence can be initiated by oncogene induction and telomere attrition, only the former can induce the formation of senescence‐associated heterochromatin foci (SAHF). To test the hypothesis that selenium‐induced senescence involves SAHF, MRC‐5 normal cells were treated with methylseleninic acid (MSeA, 0–2 μM) for 2 days, followed by a 7‐day recovery and detection of histone H3 Lysine 9 trimethylation (H3K9me3) and heterochromatin protein 1 (HP1γ), markers of SAHF. Results from immunofluorescence analyses demonstrated the expression of H3K9me3 and HP1γ foci and formation of heterochromatin in senescent MRC‐5 cells treated with MSeA. Together with our other results, we propose that the efficacy of selenium chemoprevention can be improved by targeting DNA damage response pathways in combination with chromatin modulation.