Barker, Crispin Robert Claude (Author)
Between 1935 and the early 1990s, experimental studies in medical physics, cytogenetics, biochemistry, and molecular biology produced a new, molecular interpretation of lifespan and senescence. Beginning with the discovery of artificially accelerated aging in irradiated mice and in the survivors of Hiroshima and Nagasaki, and ending with the 1990 Cold Spring Harbor studies that suggested the loss of sequences from the ends, or telomeres, of human chromosomes is the cause of senescence and cancer, this dissertation describes how aging has been reinterpreted as the result of changes in the DNA molecule and the expression of its genes. Popular histories contend that a handful of pioneering gerontologists created the molecular biology of aging. I rebut this interpretation as Whiggish, overly reductionist, and factually incorrect. I argue that the field now recognized as the molecular biology of aging did not result from the theories of a few gerontologists, but instead from large experimental programs conducted by the Atomic Bomb Casualty Commission, Atomic Energy Commission, and laboratories at major universities and hospitals. I demonstrate how, instead of being part of a continuous history, the biophysics of aging, McClintock's studies of chromosome ends, and modern telomere biology are separated by broad discontinuities. Biologists did not begin to investigate the DNA termini in the 1970s because of theories of aging or forty year-old experiments by McClintock, but to answer questions raised by two decades of basic research on ciliate macronuclear and ribosomal DNA. Likewise, the history of telomere biology itself is not a simple story of progress, in which the sequencing of the Tetrahymena telomere led directly to the discovery of the telomerase enzyme, and from there to the Cold Spring Harbor experiments linking senescence with telomeres. Instead, it is composed of separate stories, in which distinct assemblies of scientists used mouse, salamander, ciliate, yeast, parasite, and human DNA to examine divergent problems in molecular biology.
...MoreDescription Cited in Diss. Abstr. Int. A 69/06 (2008). Pub. no. AAT 3317061.
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