Senescence and the Genome

Interphase Chromosomes in Replicative Senescence: Chromosome Positioning as a Senescence Biomarker and the Lack of Nuclear Motor-Driven Chromosome Repositioning in Senescent Cells

“…Senescence can be caused by various different stimuli, and the different types of senescent cells may even have different roles within the body ( Bridger and Foster, 2021 ). In replicative senescence (RS), cells reach senescence through serial division, and are permanently arrested although metabolically active ( Hayflick and Moorhead, 1961 ).…”

“…Senescent fibroblasts possess a larger, flatter morphology ( Bowman et al, 1975 ; Sherwood et al, 1988 ), with an enlarged nucleus ( Mehta et al, 2007 ; Mitsui and Schneider, 1976 ), increased adhesion to the extra cellular matrix, fewer cell–cell contacts ( Campisi, 2000 ; Narita et al, 2003 ; Ben-Porath and Weinberg, 2004 ) and increased aneuploidy ( Benn, 1976 ; Sherwood et al, 1988 ; Mukherjee et al, 1995 ). Moreover, in recent years many studies have demonstrated alterations to the genome organisation of senescent cells ( Bridger and Foster, 2021 ). Exit from the cell cycle into senescence is also accompanied by changes in chromatin modifications ( Rai and Adams, 2013 ) i.e., methylation and acetylation ( Wilson and Jones, 1983 ; Singhal et al, 1987 ; Imai and Kitano, 1998 ; Lander et al, 2001 ; Wagner et al, 2001 ; So et al, 2006 ; Dimauro and David, 2009 ; Grandinetti et al, 2009 ) with CpG islands being globally demethylated ( Cheng et al, 2017 ) and other specific CpG islands being hypermethylated ( Cruickshanks et al, 2013 ).…”