It is becoming more and more apparent in conservation that we need a good understanding of translocation biology, and my research is working on just that. This is the moving of individuals of a species either between populations in the wild or from captivity into wild populations to boost genetic diversity. Where isolated populations have depleted either from climate change, human interference, or some other phenomenon, we have significantly reduced their genetic variability, and in doing so have reduced many populations’ probabilities of survival. With the global depletion of many species, communities, and ecosystems, we are relying more and more on translocation conservation, to introduce foreign individuals into depleted populations, boost diversity, and increase a population’s stability for the future.
Whilst translocations have been used with good intention, there has been variance in success. Whilst useful in some cases, in others, the translocation of individuals has actually led to an increased degradation of rare populations. It seems quite a simple concept, but it is becoming clear that translocations are more complicated than first thought. Important to my research, many of the complications that arise from translocations lie, at the heart, in conservation genetics.
I am looking at what happens when a foreign individual is translocated into a population and backcrossed many many times, as would occur over a number of generations in the wild. If a female is translocated into a population, its descendants down a female line will have a pretty much entirely native population autosomal DNA, but still with a mitochondrial genome from the original foreign female. The same will be true for a male translocation, but with the y-chromosomal DNA instead, and this will only be realised in the male descendants.
Particularly unique to my research, is investigating incompatibilities between the y, mitochondrial, and autosomal DNA that may arise after so many generations. Although not investigated yet, it is very plausible for these incompatibilities to arise, as the mitochondria is inherited solely down the female line without recombining with the rest of the genome during sexual reproduction. As a result, it is prone to accumulating deleterious mutations that may compromise fitness. This is ok in a normal population, though, as the rest of the genome undergoes recombination, and can evolve to produce complementary combinations of genes to compensate for any weird accumulating mutations. If that autosomal DNA is swapped, however, for a collection of genes that haven’t adapted to the mitochondria’s maladapted genes, then it cannot compensate, and the fitness of that genome will be lower than what was before despite an increased genetic diversity within a population. The same could be said here for foreign y-chromosomal DNA introduced into a population, and the rest of the genome, as that doesn’t undergo recombination really, either, but is passed down the male line instead.
So that was a lot of explaining, but I hope that gives you the gist of the issue. Individuals crossed so many times in a population will end up with either a y-chromosome or mitochondria from one population against the rest of the DNA from another population. As a result, the genome may not be fully complementary in a way that compensates for accumulated deleterious mutations. Furthermore, the mitochondrial and y-chromosomal DNA cannot be purged out of the genome through recombination, and so the individual will contribute less-fit individuals to an already depleted population, making the increased genetic diversity a hindrance to the population’s stability. These are the exact interactions that I am investigating, and I am doing it with Drosophila melanogaster!
Whilst many experiments have investigated incompatibilities between closely related species, giving evidence for a mechanism of speciation, no experiments have investigated these incompatibilities described above within a species. Here, I’m using distinct and locally adapted species from different locations across the globe, with temperature differences to represent different local adaptations to different local climates that the populations were sourced from. Ultimately, I am hoping to find out how important these incompatibilities really are in determining a population’s fitness.
I have spent many months creating the kind of crossed individuals that I need to investigate these probable fitness impairments as a result of translocations, and I am now undertaking lots of fitness tests to see how they compare to the uncrossed pedigrees. My locally adapted and distinct fruit fly populations come from Bizerte in Tunisia, South Wootton and Nottingham in England, and Tahiti.
If successful then this may be the first experiment to find such incompatibilities between locally adapted populations, despite it being suggested as a source of translocation failure before. If successful, then we may well have found a new and exciting bit of science that will guide translocation conservation in many years to come – not too bad for an experiment in the trusty Drosophila melanogaster!
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