Research

I am in the process of updating this page! Here you will see flavours of my past work.

 

Sex-specific mitonuclear epistasis

Mitochondria are cells’ powerhouses involved in metabolism, cellular signalling and regulating cell death. Mitochondrial function depends on a close interaction between its own few, but vital, genes and hundreds of nuclear encoded genes. This sets the stage for widespread epistasis between the two genomes. We are particularly interested in the implications of maternal inheritance of mitochondria on the evolution of sex-spefic phenotypes that depend on mitochondrial function. Only females pass on the mitochondria to their offspring, and therefore the mitochondrial genes can experience an evolutionary change in response to selection only through females (except in some restricted circumstances). For males the maternal inheritance implies putative constraints for adaptive evolution of male-limited phenotypes. However, the nuclear encoded mitochondrial genes provide a large target for male-specific selection to influence mitochondrial function. All of this together predicts sex differences in the epistatic interactions affecting sex-limited phenotypes.

We are testing this for female and male reproductive, physiological, life-history and personality (study led by Hanne Lovlie and already published) traits, using mitonuclear introgression lines that mix and match different mitochondrial haplotypes to be expressed on different nuclear genetic backgrounds using C. maculatus.  In particular, we are currently studying how mitonuclear epistasis shapes sex-specific reproduction through life because mitochondria have been implicated in ageing in many ways in previous research. Metabolic demands specific to male reproductive phenotypes should also be a hot spot for such effects and therefore we are interested in how mitonuclear epistasis influences male metabolic rate associated with ejaculate renewal and other post-mating processes.  Our work also involves experimental evolution approach to test how mitochondrial genetic variation and mitonuclear epistasis influence sex-specific adaptation to new environments.

Costs of reproduction

One of the key concepts in sexual selection theory is that optimal mating strategies for each sex depend on the costs of reproduction. Costs arise from the economics of optimal use of limited resources, but also due to sexual conflict between the mating partners. In order to better understand mating system evolution we use a comparative approach to study how the costs and benefits of investment into reproduction differ across related species. We are testing how they depend on mating rate, and may thus originate from sexual conflict, and have shaped inter-specific variation in morphological and physiological traits involved.

Sex differences in gene expression

Females and males share the same genome (apart from the sex chromosomes), but yet show marked sexual dimorphism across both reproductive and somatic traits. One of the key ways through which they achieve this is sex- and tissue-specific regulation of gene expression. Recent evidence (including my own work with Mike Ritchie and Rhonda Snook) show how sex-biased gene expression can evolve rapidly under different mating systems, which posits such genes as candidates to further our understanding of how sex-specific selection operates at the genetic level. We are quantifying sex-biased gene expression using de novo RNA-seq and how it changes due to mating in order to identify such candidate genes in C. maculatus.

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