Telomeres in relation to aging How to test whether aging is related to telomere function, or non-function. Evidence is better for a relation of telomeres to tissue culture cell "Senescence". "Immortal" cell lines like HeLa and L-cells have very active telomerase enzymes. Tissue cultures started from embryonic tissues die out after 50-70 cycles of growth to fill Petri dishes. When tissue cultures were started from elderly mice, rats or people, then it was reported that this dying out would occur after a smaller number of cycles of growth and transfer. "Senescent" tissue culture cells would be expected either to lack the usual numbers of telomeres (some chromosomes would be missing them), or have much shorter chains of repetitive base sequences on the ends of some or many other their chromosomes. "Senescent" tissue culture cells would lack or have reduced amounts of proteins whose genes map near the ends of chromosomes. Tissue culture cells from many different species of animals could be compared, looking for correlations between genes that map near the ends of chromosomes (in some kinds of animals, but map nearer the middles in other kinds of animals) versus biochemical abnormalities of senescent cells of each species. Different biochemical and structural abnormalities should occur in animals with genes A, B or C mapping near chromosome ends, as compared with species in which the equivalent genes map far away from ends. Transforming extra copies of genes for telomerase into cells should be able to produce immortal cell lines. Tissue cells started from cancers (especially fast growing cancers) should be able to grow and divide in culture without limit, and either delay senescence until more doublings of populations, or never senesce. Slowing rates of growth and division of tissue culture cells (by providing reduced amounts of growth factors, or using special substrata, or any treatment that would slow growth without harming the cells) would tend to allow the rates of functioning of telomerase enzymes to keep up with the rates of cell growth and chromosome duplication, with the result that cells could undergo more doublings before senescence would occur. Over-stimulating cell growth and division should tend to cause senescence to occur after a smaller number of cell cycles.