Evolutionary Solutions to Diseases

Our research in this area mainly relates to mitochondrial malfunction, leading to disease in humans and animals, including myopathies, neuropathies, metabolic diseases, and infertility. Substantial evidence suggests it may not always be the faulty mitochondria per se that cause the disease but a disrupted interaction/ communication/ signalling between the mitochondria and the nucleus. This evidence is largely based on experiments in animals and on the observation that not all people with a particular mitochondrial mutation develop the disease – some nuclear backgrounds seem to cope with faulty mitochondrial mutations. We have developed experimental systems, so-called Drosophila mitolines, that allow us to quantify the health and fitness effects of different mitochondrial-nuclear matches. The resulting data have substantial bearing on the recently introduced mitochondrial replacement therapy, where nuclear DNA is placed into unrelated mitochondrial surroundings.

Second, the dichotomy of death vs. survival, or expression vs. no expression of a phenotype, of gene-depleted mutants is not a good representation of the health effect this gene confers. We favour the concept to measure health effects as the relative competitive disadvantage against a control group.

Topics for Master theses are available here.

See our publications on this topic:

Morrow et al. 2015. Risks inherent to mitochondrial replacement. EMBO Reports, DOI 10.15252/embr.201439110. link to pdf

Dobler et al. 2014. A meta-analysis of the strength and nature of cytoplasmic genetic effects. Journal of Evolutionary Biology 27: 2021-2034. link to pdf.

Reinhardt et al. 2013. Mitochondria replacement, Evolution, and the Clinic. Science 341: 1345-1346. link to pdf

Reinhardt 2014. Wechselwirkungen zwischen dem Erbgut von Mitochondrien und Zellkern. Naturwissenschaftliche Rundschau 67: 123-127. link to pdf

Here is some coverage. Note, that not everyone is happy with our conclusions: