Mitochondria are fascinating organelles that have achieved fame on the internet as the ‘powerhouse of the cell’, producing 90% of the cell's energy in the form of ATP. Based on this essential role, it is thought that differences in mitochondria determine the strengths and weaknesses of individuals and even entire species. As a result, there's interest in trying to understand how the environment and genetics shape mitochondrial function. In their recent study, Antoine Stier from the University of Turku, Finland, and colleagues from the University of Glasgow, UK, incubated Japanese quail eggs (Coturnix japonica) at different temperatures and studied changes in how their mitochondria performed from early-life into adulthood. They wanted to know whether animals can adjust how their mitochondria perform, depending on the temperature they experience before birth, and whether these changes are maintained as they develop into adults.

The scientists incubated Japanese quail eggs at high (38.4°C), medium (37.7°C) and low (37.0°C) temperatures – a temperature range that maximizes differences in how quickly embryos grow. They also included an unstable temperature treatment (dipping briefly, several times, to 29.5°C from 37.7°C) to mimic when the mother leaves the nest to forage. When the chicks hatched, the researchers transferred the animals to 21°C as they grew, collecting blood samples at 20 days of age and at 60 days to investigate how the mitochondria in the blood cells were affected by the temperature at which the chick embryos developed and how they changed after the chicks hatched and grew into adults. The team measured the oxygen consumption rate of the mitochondria, which is tightly linked with the amount of ATP these structures can produce, the amount of DNA damage they had incurred and the length of the telomere structures that cap chromosomes – which shorten with age.

The team found that the oxygen consumption rates of the mitochondria of the chicks incubated at 38.4°C were higher than those of the chicks from colder eggs, probably because the embryos in the warmer eggs developed faster and needed more energy to support their rapid growth. In addition, the mitochondria of the adult quails that had developed in hot eggs had higher oxygen consumption rates, meaning that this increase was not temporary and that the thermal environment that these birds experience as an egg shapes their ability to produce ATP throughout their lives. But the blood cells with mitochondria that consumed oxygen faster only had a small increase in the amount of DNA damage and no change in telomere length – which is surprising because overactive mitochondria that consume more oxygen can produce toxins that damage DNA and cause aging.

As the adult birds aged, their mitochondrial oxygen consumption decreased, probably reflecting the extreme energy demands they experienced as they grew rapidly during the first 20 days after hatching. When the team checked the oxygen consumption rates of the mitochondria of the birds that were incubated at unstable temperatures – as if their mothers kept wandering off – they found they were similar to those of birds incubated at a constant 37.7°C. This tells us that when the environmental temperature is unstable, these birds use the temperature that they experience the most as the cue to program their mitochondria throughout life.

The role that the environment a developing embryo experiences has on programming mitochondrial function after birth is a research area with major implications for human health and conservation efforts. Stier and colleagues have shown that something as simple as increasing incubation temperature can cause a change in mitochondrial function that persists into adulthood. Understanding how these changes in mitochondrial function come about and whether they are important for improving whole-organism performance and ultimately survival will be critical areas of future research.

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Experimental demonstration of prenatal programming of mitochondrial aerobic metabolism lasting until adulthood
Proc. R. Soc. B