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Genetic Self-Destruction – Some worms that are programmed to die early for the sake of the colony

Some worms are genetically predisposed to die before age, which the colony apparently benefits by reducing food requirements. This was the result of a new study by University College London.

The model study, published in Aging cellprovides the first evidence of programmed, adaptive death in an animal that has evolved due to the benefits to the community.

Lead author Professor David Gems (UCL Institute for Healthy Aging) said: “According to the theory of evolution, altruistic death cannot normally develop to give your relatives more food. This is because other people who live longer would consume resources left behind by altruistic comrades and surpass them in a so-called community tragedy.

“But it was recently discovered that wild C. elegans Roundworms live in colonies of identical worms, which would prevent long-lived worms with different genes from taking control. “

The researchers explain that evolutionists originally believed that aging had developed to reduce the population in order to increase food availability for the boys. Since then, scientists have shown that this cannot be the case for most animal species, since longer-lived non-altruists are usually preferred by natural selection.

However, certain organisms appear to have self-destruction programs that prevent them from living beyond a certain age. For example in the tiny roundworm C. elegansMutations in certain genes can massively extend their lifespan, presumably by switching off the life-shortening program.

In the current study, UCL researchers examined the peculiarities of C. elegans Life cycle to understand why programmed death can work for them by developing computer models of a C. elegans Colony grows on a limited food supply. They tested whether a shorter lifespan would increase the fertility of colonies by producing the equivalent of colony seeds (a form of spreading the worm called duration).

They found that shorter lifespan, shorter breeding times, and a reduced feeding rate in adults increased the colony’s reproductive success.

The first author Dr. Evgeniy Galimov (UCL Institute of Healthy Aging) said: “It has been known for years that programmed cell death has benefited living organisms, but we are now realizing that there is also a programmed organismal death that can benefit animal colonies.”

The results have a significant impact on studies of the biology of aging, much of which is done using C. elegans. Other animals have genes that are similar to genes that shorten lifespan and promote disease in late life. A better understanding of the function of the genes could therefore contribute to medical research.

However, the researchers warn that their latest findings are specific to worms whose life cycles are suitable for such an adaptation mechanism.

Professor Gems said: “Our results are in line with the old theory that aging is beneficial in one respect, as it shows how increasing the availability of food for your relatives through premature death can be a successful strategy, which we call consumer sacrifice. However, adaptive death can only develop under certain special conditions, under which populations of closely related people do not mix with non-relatives. So it is not predicted that this will apply to humans, but a lot seems to happen to colonial microorganisms. “

Dr. Galimov continued: “It seems possible that some types of salmon that spawn and die in large numbers in the upper reaches of rivers can die adaptively. It has been shown that the rotting, dead salmon fries the salmon. We call this form of the adaptive victim of death biomass. “

The work shows how reducing the evolutionary fitness of individuals can improve the fitness of communities in organisms living in colonies.

The authors say that the next step in their work is to study the actual C. elegans Colonies to test for behavior predicted by the model and then use this knowledge to create more realistic models to understand adaptive death.

Reference April 17, 2020, Aging cell.
DOI: 10.1111 / acel.13141

This work was funded by Wellcome with support from the BBSRC.

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