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Antagonistic Pleiotropy Theory

Database
Antagonistic Pleiotropy Theory

Author:

G. Williams

History:

The antagonistic pleiotropy theory of aging was first proposed by G. C. Williams in 1957. Essentially, this theory is close to the mutation accumulation theory of aging.

Example:

There is a number of antagonistically pleiotropic genes including genes acting in insulin signalling or genes taking part in the synthesis of lipophilic hormones. The genes mentioned above have dual function. On the one hand, they stimulate growth and reproduction. On the other hand, they suppress stress resistance and so they precipitate senescence.

Description of the Theory:

According to this theory, aging is connected with antagonistically pleiotropic genes. That sort of genes control for more than one trait where at least one of these traits increase organism’s survival potential or reproduction at the early stages of life and at least one trait bring mentioned characteristics down at the late stages of life. The dual effect of such genes is known as «antagonistic pleiotropy». Antagonistically pleiotropic genes are maintained in populations by natural selection as their early benefits outweigh their late harm.

Data of modern molecular genetic analysis confirm the antagonistic pleiotropy theory. A lot of antagonistically pleiotropic genes were revealed. One of them is p53 gene that is a tumor suppressing gene and, at the same time, the gene participating in cell aging.

The antagonistic pleiotropy theory predicts that rapid development of an individual will correlate with rapid aging because the faster puberty is attained — the earlier senescence begins. The theory gives one more prediction: selection towards life-span extension lead to lowering of early fertility.

Additions:

The antagonistic pleiotropy theory is close to the mutation accumulation theory of aging. The chief distinction between these theories is that, in mutation accumulation theory, genes with negative effects are passively cumulated from one generation to another, while in case of antagonistic pleiotropy this sort of genes is supported in population by the force of natural selection. Nevertheless, these theories are not incompatible. Both of the proposed evolutionary mechanisms may occur simultaneously.

Сriticism:

Existence of sexual selection in elderly age. Though the natural selection diminishes in elderly age, the evolution will promote the selection of genes important for the reproduction at an early age in rare cases only. For example, permanently changing, aggressive environment will give advantages to antagonistic pleiotropy. Nevergheless, in actual stable society where there is no abrupt changes and aggressive environment, a tendency exists to have children in later life. In this case, genes promoting healthy longevity and increasing reproductive age will be selected.

Great variability in life-span between related organisms. Thereby, though related organisms have identical or similar sets of genes, their life-span may be far too different.

Resume:

This theory allowed G. Williams to make a prediction about negative correlation between life-span and reproductive potential.
The theory works but it is necessary to amplify it with other theories.

Publications:

  • Williams GC: Pleiotropy, natural selection, and the evolution of senescence. Evolution 1957;11:398–411.
  • Zahavi A: Mate selection: a selection for a handicap. J Theor Biol 1975;53:205–214.
  • Krtolica A, Parrinello S, Lockett S, Desprez PY, Campisi J: Senescent fibroblasts promote epithelial cell growth and tumorigenesis: a link between cancer and aging. Proc Natl Acad Sci USA 2001;98:12072–12077.
  • Cutler RG, Semsei I: Development, cancer and aging: possible common mechanisms of action and regulation. J Gerontol 1989;44: 25–34.
  • Economos AC, Lints FA: Developmental temperature and life-span in Drosophilamelanogaster. 1. Constant developmental temperature: evidence for physiological adaptation in a wide temperature-range. Gerontology 1986;32:18–27.