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Why Longevity is Extended by Restricting Food Gets
New Look
Researchers find new genes that control longevity
Nov. 23, 2005 – Scientist have long known that
restricting food intake in animals will increase their longevity by as
much as 40 percent. A new model for how this happens is emerging from
studies led by Howard Hughes Medical Institute researchers who have
identified 10 new genes that regulate longevity in yeast… and maybe in
higher organisms.
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The results of the studies are important, the
researchers say, because they begin to provide an explanation for the
“life extension” effect seen in laboratory animals when food is
restricted. So the studies could offer new clues about the molecular
mechanisms that living organisms employ when food is scarce, said
Fields.
Although it seems counterintuitive, experiments
showed long ago that severely restricting food intake leads to an
increase in longevity - by as much as 40 percent — in some animals.
Although the longevity phenomenon was well documented in laboratory
animals, researchers remained unsure about how it happened.
Now, these new experiments are uncovering some of
the molecular pathways that are involved in controlling longevity in
yeast, and thus probably in more complex organisms.
Molecular biologists Matt Kaeberlein, Brian
Kennedy, Stanley Fields, and colleagues at the University of Washington,
reported in the November 18, 2005, issue of the journal Science that by
decreasing the function of nutrient-responsive pathways such as TOR and
Sch9, the life span of yeast is extended. Fields is a Howard Hughes
Medical Institute investigator at the University of Washington.
“Even though yeast is a simple, single-cell organism, it’s still capable
of revealing mechanisms in the aging process. Similar genes may control
aging in higher organisms, too.”
Stanley Fields
“Through a large-scale screening process we have
identified a set of genes that slows aging in yeast.” Kaeberlein
explained. He and his colleagues are hoping to use that model to expand
their understanding of longevity higher up the evolutionary ladder, even
into humans. “We speculate that it is important in higher organisms,”
Fields added, since very similar genes are found in most other species,
from worms to fruit flies, mice and humans.
The next step, Kaeberlein said, is to begin similar
work in the nematode worm, Caenorhabditis elegans. After that, they hope
to study the process in mice, and eventually in humans — all with the
goal of understanding the aging process.
Although it is unlikely to happen soon, the
discoveries may eventually identify targets that can be manipulated —
perhaps by drug treatments — to alter the aging process, Fields said.
One drug, rapamycin, is already known to impact one of these genetic
pathways, but it has the dangerous side effect of disabling the immune
system.
“We'd like to understand how aging occurs in
yeast,” Fields added, because “even though yeast is a simple,
single-cell organism, it's still capable of revealing mechanisms in the
aging process. Similar genes may control aging in higher organisms,
too.”
The two years of laboratory work, much of it done
by Kaeberlein and Kennedy, were extraordinarily tedious, involving
complex genetic and biochemical tests on a special collection of 4,800
strains of yeast cells developed by other scientists. Each yeast strain
was engineered to be special, and different, by lacking a different
gene.
One of the group's most challenging tasks involved
segregating 564 yeast strains into three categories: short-lived, not
long-lived, and long-lived. Such work involved careful examination of
tens of thousands of individual yeast cells under the microscope,
separating “daughter cells” from “mother cells,” and segregating strains
according to longevity.
In yeast, aging is measured by counting
“replicative life span,” the number of daughter cells produced by a
given mother cell before senescence. In the experiments published in
Science, researchers categorized cells as not long-lived if the mean
life span was less than 26 generations. If the mean life span was less
than 20 generations, those yeast strains were put in the short-lived
category. Finally, if the mean life span was greater than 36
generations, then those strains were called long-lived.
In time, the researchers gradually sorted out some
gene mutations that altered the life span of the cells. As a result,
“ten new genes were identified that are connected to longevity, and six
of them are implicated in a single pathway” in the cell's response to
nutrition, Fields explained.
For example, one gene they identified, called TOR1,
seems to regulate yeast's response to nutritional conditions. When the
gene is mutated, and not working properly, the yeast undergo a
starvation response similar to that of calorie-restricted cells - even
when nutrients are abundant. The acronym TOR stands for “target of
rapamycin.”
What's also clear is that these genes don't work
alone. TOR and its relatives are active in networks. Fields and his
colleagues are trying to identify and analyze other parts of such
systems.
“Our hope is that this will lead us to the
mechanisms involved in caloric restriction and life extension,”
Kaeberlein said.
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