Research

Current Research:
Sex differences, Metabolism and Mitochondria
Max Reuter Lab
Males and females perform different reproductive roles and have adapted to these by evolving sometimes strikingly different phenotypes. A key means to observe and understand differences is to examine metabolism, with studies being able to link differences in diet composition to varying levels of phenotypes. In spite of the clear dimorphism observed across the animal kingdom, both sexes are locked into a struggle over adaptation, rooted in the fact that both sexes share an almost identical genome. Here, I aim to combine high-throughput phenotypic approaches (including quantitative genetic tools), with cutting-edge genome expression data to identify genes and genetic pathways that are involved in metabolic conflict. My first aim is to explore whether males and females differ in dietary preference using Drosophila melanogaster as a model organism. I aim to establish the extent to which genetic correlations between male and female food preferences constrain the evolution of optimal diet choice. Consequently, my second aim is to identify genes and/or genetic pathways that are responsible for differences in diet preference, and limit the dietary adaptation. Finally, I aim to use state-of-the-art genetic manipulations to enhance/suppress parts of the genetic pathways involved in metabolism, and will examine if these genetic modifications bring sex-specific consequences to the physiology of the organism. Understanding the genetic basis for sex differences in metabolism will aid to build complete understanding of the differences between males and females at the cellular level and provide insight into dietary and metabolic influences as well as aid human health research.

Mitochondrial work @ UCL
Being at UCL has put me in contact with some great mitochondrial aficionados. In collaboration with Nick Lane we are exploring the effects of the mitochondrial genome in a tissue-specific manner. We are interested in metabolism and cytoplasmic male infertility using Drosophila melanogaster as a model species.

With François Balloux we are interested in exploring the effects of the mtDNA genome on human migration patterns and see if this small genome has helped humans adapt to different environments.


PhD Research ( @ Damian Dowling Lab ):

The mitochondria are essential for life in eukaryotes, taking centre-stage in the process of cellular respiration. This process is regulated via a series of finely coordinated interactions encoded by two obligate genomes – nuclear and mitochondrial. Both genomes are required for the production of cellular energy, and thus their harmonious interaction is vital for the maintenance of mitochondrial integrity and the viability of eukaryote life. Recently many studies have shown an abundance of phenotype-changing genetic variation segregating within the mtDNA genome – and these results run counter to the traditional paradigm in which mitochondrial genetic variation was expected to be evolving neutrally. It remains unclear how this variation is accumulating – either adaptively under selection, or non-adaptively under mutation-selection balance. Furthermore, maternal inheritance of the mitochondrial genome predisposes this genome to accumulation of mutations that have male biased effect, and the existence of these male-harming mutations has recently been empirically substantiated.

The aim of my PhD thesis was to explore and elucidate the nature of the evolutionary processes that shape the molecular architecture of the mitochondrial genome. My goal was to understand how much of the genetic variance accumulating within the genome is sex-specific, and in particular male-biased. This would support the idea that mitochondrial variation consisted largely of deleterious mutation loads that accumulate under maternal transmission. Secondly I was interested in understanding how much genetic variation is adaptive – occurring in both sexes, and exhibiting phenotypic responses to thermal stresses that concord with expected predictions based on where the mtDNA genotypes have evolved. Finally, I aimed to elucidate the molecular mechanisms that bridge the link between mitochondrial genotype and phenotype.


Excellent video explaining our mitochondrial scientific findings from 2012:


Click HERE for my 2013 ESEB talk

Here is my: Google Scholar 

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