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Aisin, S. I.

Publications and source records attributed to Aisin, S. I..

2 recordsLinked to original sources

Social immunity as a driver of life-history evolution in eusocial species

Eusociality is accompanied by puzzling lifespan phenotypes that challenge classic theories of aging. In eusocial species, breeders age more slowly than non-breeders while sharing the same genomes. A notable exception is the naked mole-rat, in which all castes show negligible actuarial senescence. We show that both patterns can be explained with a single epidemiological model. Chronic parasites that reduce worker productivity can drive the evolution of shorter lifespan in workers, but not in queens. A genetic program that triggers the death of infected workers can evolve as an efficient alternative strategy for controlling pathogens, thereby reducing selection for shorter lifespan. However, in the presence of benign pathogens, this program results in excessive deaths and becomes too costly. Therefore, the composition of the pathogen mixture defines optimal life histories in eusocial communities: species exposed to a broad pathogen repertoire evolve caste differences in lifespan, whereas species occupying pathogen-poor environments are predicted to die rapidly upon infection and experience negligible aging. This framework links social immunity to life-history evolution and yields testable predictions for the pathogen control hypothesis of aging.

evolutionary biology↗

Avoidance Of Rejuvenation: A Stress Test For Evolutionary Theories Of Aging

The biological feasibility of human rejuvenation remains a subject of intense debate, yet answering this question is critical for guiding research strategies. Should aging research focus on reversing aging in older individuals, or on pausing its progression at earlier ages? We address this question with evolutionary biology. Classic evolutionary theories of aging-- damage accumulation, antagonistic pleiotropy, and the disposable soma--consider aging as a detrimental byproduct of evolution. From this perspective, rejuvenation should confer strong fitness advantages and therefore be expected to evolve in species experiencing substantial aging in the wild. Its rarity in nature should thus be interpreted as evidence of its mechanistic implausibility. Yet, rejuvenation does occur in a few species, and, paradoxically, it is typically induced by stress but not used under optimal conditions. Using mathematical modeling of lifespan plasticity in eusocial insects, we show that this pattern cannot be reconciled with classic theories of aging, revealing an internal contradiction between these theories and the observed avoidance of rejuvenation. By contrast, the pathogen control hypothesis--which interprets aging as an adaptive, programmed process--offers a consistent evolutionary framework for understanding and potentially achieving rejuvenation.

evolutionary biology↗