The research, published in the journal eLife, shows why Killifish accumulates harmful mutations that cause age-related diseases that shorten life expectancy. This could help scientists better understand how human life expectancy among the population is increasing and lead to a new understanding of the problem of human aging.

Killfish are any of the various oviparous carp fish. In total, there are about 1270 species of killifish, the largest family of which is Rivulidae, containing more than 320 species. The very short life span of turquoise Killiph fish – three to nine months – makes them an ideal model for studying aging. Killiphs live in temporary ponds in Africa that dry out for part of the year, which means they must hatch, mature, and reproduce before that happens. Their eggs survive dry spells in a state similar to hibernation and hatch when the rains fill the pond again, giving rise to a new generation.

“Different populations of wild turquoise killiph fish have different lifespans, and we wanted to investigate why,” explains lead author David Willemsen, Research Fellow at the Institute for the Biology of Aging. Max Planck, Cologne, Germany.

As part of their research, Willemsen and senior author Dario Riccardo Valenzano carried out fieldwork in Zimbabwe’s savannah basins to capture and collect samples of the Killiph genome for sequencing and analysis in the laboratory. The team then compared the genomes of killyphs living in the driest environments, who have the shortest lives, with those of killyphs from more humid environments, which live several months longer.

Short-lived Killiphs have very small, often isolated populations, resulting in so-called “cramped habitats,” which the team has found a lead to the accumulation of harmful mutations in their populations. In contrast, longer-lived killyphs have a larger population, and new fish with new genetic material is often added to their populations. Over time, these larger populations allow natural selection to more efficiently remove harmful mutations.

“The limited population sizes caused by habitat fragmentation and repetitive tight habitats in populations increase the likelihood of harmful mutations accumulating in the population,” says Willemsen. “Our work can help answer a key question about aging by suggesting that population dynamics, rather than evolutionary selection for or against certain genes, contributes to the accumulation of deleterious mutations that lead to aging and shorten life.”

“Harmful mutations accumulate passively in killer populations, and this is even more noticeable in smaller populations that live in drier conditions,” says senior author Dario Riccardo Valenzano, team leader at the Max Planck Institute for Biology and Aging. “Our results highlight the role of demographic constraints in shaping longevity within species and could potentially be expanded to provide new insights into aging in other animal and human populations.”