As a companion piece to recent work on histones and aging in yeast, these researchers investigate further the connections between cell aging and histones: "as cells count down to senescence and telomeres wear down, their DNA undergoes massive changes in the way it is packaged. These changes likely trigger what we call 'aging'. ... Prior to this study we knew that telomeres get shorter and shorter as a cell divides and that when they reach a critical length, cells stop dividing or die. Something must translate the local signal at chromosome ends into a huge signal felt throughout the nucleus. But there was a big gap in between. ... [researchers compared] levels of proteins called histones in young cells - cells that had divided 30 times - with 'late middle-aged' cells, which had divided 75 times and were on the downward slide to senescence, which occurs at 85 divisions. Histone proteins bind linear DNA strands and compress them into nuclear complexes, collectively referred to as chromatin. ... aging cells simply made less histone protein than do young cells. ... These proteins are required throughout the genome, and therefore any event that disrupts this production line affects the stability of the entire genome. ... Comparisons of histone patterns in cells taken from human subjects-a 9- versus a 92-year-old-dramatically mirrored histone trends seen in cell lines. ... These key experiments suggest that what we observe in cultured cells in a laboratory setting actually occurs and is relevant to aging in a population." This might be thought of as another line of evidence in the debate over the degree to which nuclear DNA damage contributes to aging.