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| What does research on other animals and organisms
tell us about the human aging process? |
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What have we learned from animal models of
aging about DNA damage? |
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Damage to our genes and DNA undoubtedly plays a role in aging. Our genes
are strung together in long chains of DNA (deoxyribonucleic acid). When
a cell divides, it must first double its DNA in the process of replication,
so that each daughter cell receives a full complement of it. Our genes
are responsible for the production of the proteins that do much of the
work of our cells and bodies. The processes of copying genes for reproduction
or translating them into proteins are very complex, and the potential
for mistakes to occur is high. Our cells have therefore evolved extensive
mechanisms for the repair of DNA, involving a variety of proteins that
recognize damaged DNA and remove the mistakes. All living creatures have
multiple genes (segments of DNA) that produce proteins whose job it is
to repair DNA. One method of DNA repair includes the use of "checkpoints"
--if the DNA has been damaged near that checkpoint, the cell recognizes
it and either stops reproducing or turns itself toward apoptosis, a genetically
programmed death of that cell.
Research into DNA repair mechanisms has revealed some interesting parallels
between those found in animals and those found in humans. Some of that
research includes:
 Yeast
Roundworms
Fruit
flies
Mice
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Yeast |
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One aspect of DNA repair is called checkpoint control, and in yeast, the
longevity gene RAS2 plays a role in checkpoint control. Another gene called
RAD52 also affects yeast life span. It is also involved in DNA repair,
in the area of recombination repair.
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Roundworms |
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Genes have been identified that block cell death after DNA damage.
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Fruit flies |
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DNA damage plays a role in certain human diseases. Some of the most well
studied human diseases that can be attributed to defects in the repair
of damaged DNA are xeroderma pigmentosum, Cockayne syndrome, and trichothiodystrophy.
People with these diseases are very sensitive to damage induced by ultraviolet
light. The genes responsible for much of the damage of these diseases
have counterparts in fruit flies. Researchers hope that a greater understanding
of the fruit fly versions of these genes will lead to a greater understanding
of the human diseases.
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Mice |
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Scientists have bred mice that develop the mouse version of xeroderma
pigmentosum. Like their human counterparts, the mice have defects in their
DNA repair mechanisms due to specific gene abnormalities. Because the
skin of these mice is so sensitive to ultraviolet light, they are especially
good models for the study of the effectiveness of various sunscreens.
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