Quiz
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1. What does the somatic mutation theory claim?
That aging is caused by mutations arising in the cells of the body during life. Szilard, 1959, called them aging hits (Figure 1).
2. How is Medawar's mutation accumulation different?
It is about inherited mutations that act late and remain in a population because selection is weak by then. It is not a count of mutations inside one body (Figure 1).
3. What did Williams 1957 propose?
Antagonistic pleiotropy: a gene that helps early and harms late can be favored. It is not the somatic mutation theory, and it is not Medawar's mutation accumulation (Figure 1).
4. What became of Orgel's error catastrophe?
The strong form predicted rising protein-synthesis errors. Harley and colleagues, 1980, did not find that rise in cultured human fibroblasts, including Werner cells. The test is cells in a dish (Figure 1).
5. What did Cagan and colleagues measure, and what did they find?
Single-base substitutions per year in intestinal crypts of 15 mammal species. Humans about 47 per year, mice about 796. The rate runs inversely with lifespan, and the end-of-lifespan burden varies only about 3-fold (Figure 2).
6. Why do the giraffe and the naked mole-rat matter on that chart?
Similar rates, about 99 and about 93 per year, and similar lifespans, 24 and 25 years in the paper's rounding, despite around a 23,000-fold difference in adult body mass (Figure 2).
7. What is the difference between DNA damage and a mutation?
Damage is a lesion, and it may be repaired. A mutation is a sequence change that remains. An unrepaired lesion can also stall the cell without a new sequence being written (Figure 3).
8. What did Jaiswal and colleagues find in blood?
Clonal hematopoiesis, mostly DNMT3A, TET2, and ASXL1, in 9.5 percent of people aged 70 to 79, associated with blood cancer, death, coronary disease, and stroke (Figure 3).
9. Why is the theory still contested?
A simple gene-inactivation story looks short of mutations in ordinary tissues. Heterozygous mitochondrial mutator mice carried a 500-fold higher point-mutation burden without a significant lifespan cut. Nuclear proofreading mutants died of cancer, not of a described progeria. Progeroid syndromes copy only some of normal aging (Figure 4).
10. What do the reading-room pages not show?
They do not show that a blood-cell clone, a mouse diet, or a whale protein produced the historical rise in population life expectancy. Associations stay associations, and the mouse and cell results stay in mice and cells (Figure 5).