Research.
See Also: Collaborations
Sex and Death
Forty years ago, Turner asked a pivotal question “Why does the genotype not congeal?” pondering on the paradoxical role of recombination and the persistence of variation in populations in the face of relentless natural and sexual selection. The Superfly Lab has explored this question from a variety of different perspectives, in theory and using of the Drosophila model for experiments: tradeoffs between the fitness traits that make up the life history, the role of sexual recombination in “shuffling the deck”, the input of new mutations to the gene pool and the manifold consequences of separate sexes.
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We draw upon that knowledge and incredible range of investigative tools available with the Drosophila model to answer fundamental questions about evolution by doing evolution. Using large populations of these small insects, we set up the conditions for evolution and watch it unfold. Current research falls into two broad categories: Sex & Death.
Sex includes the coevolutionary relationships between females and males – conflict and cooperation – and the differences (dimorphisms) this creates. It also includes the multifarious relationships between reproduction and survival, highlighting the fact that these research themes are strongly intertwined.
Death relates to understanding the mechanisms underlying the evolution of ageing: why do animals and plants decline in function and perish? It turns out that sex has a lot to do with it, not only by creating tradeoffs between reproduction and survival, but by creating a germline/soma dichotomy in multicelled organisms.
Sex
What would the world look like without sexual reproduction? It would certainly be a world without the splendour of flowers, the songs of birds, fierce contests for mates, and many other beautiful and brutal traits we see in the biotic world. But it might not even be a world with complex animals and plants as we know them, since the integration of cells into organisms seems to have depended upon the ability to create genetically-varied offspring in the face of armies of fast-evolving microbial pathogens. Sexual recombination was also likely a response to a pivotal event in the evolution of multicellularity: the endosymbiosis of a bacterium by a larger archaean cell billions of years ago. The relationship that resulted – between the nascent mitochondrion (mt) and the new eukaryotic cell type – forever cemented a fundamental sexual conflict over control of the cytoplasm and its occupants.
With most sexual species having two sexes – one investing in fewer, well-provisioned gametes, and the other in many, poorly-provisioned ones – the stage is set for divergence in reproductive strategies beyond eggs and sperm. Our work has documented the evolution of sexual dimorphism in morphology and life-history traits, and the malleability of sex roles in reproduction. A long term focus of the lab has been conflicts over shared traits and shared genes: Intralocus Sexual Conflict (IaSC). IaSC comes about because the two sexes make use of a common genome, yet are often selected in different directions creating a “tug of war” over the shared genes. IaSC is not just an intellectual concern, it sustains genetic diversity and is the driver of many genomic imprinting processes – processes that result in an array of diseases and disabilities when imprinting goes wrong.
Four main themes drive our research program on the evolution of sex: (1) The adaptive significance of sex, (2) sexual conflict, (3) sex differences and sexual dimorphism, and (4) the evolution of sex chromosomes and other genomic adaptations to sex.
Current Projects
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Intralocus Sexual Conflict [Harsha]
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Sexual Selection and Sex Roles under Demographic Pressure [Josh & Simmal]
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Cytonuclear Coadaptation [Celina & Naida]
[example of protocols and results]
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Death
Evolution allows for organisms that have reached maturity through a complex process of growth and development to then decline in performance, wither, and die. Why does selection allow organisms to senesce? The Evolutionary Theory of Ageing (EtoA) explains this as the decline in the force of natural selection with age after maturity. Simply put, evolution cares more about young organisms than older ones, leading to two specific predictions for “ageing genes”: first, genes with beneficial effects early in life can be selected for, even if they have negative effects later in life; this is the Antagonistic Pleiotropy (AP), or “live fast, die young” hypothesis, that predicts tradeoffs between early and late performance. Second, genes (e.g., mutations) with late age harming effects are more likely to build up in populations than genes causing harm early in life; this is the Mutation Accumulation (MA) hypothesis. There is good evidence for both AP and MA in the evolution of ageing. For example, there are many diseases with late-age onset, like Huntington’s chorea, which have already been passed on to offspring before parents begin to show signs of illness; natural selection is weak against such genes.
The MA hypothesis has largely been developed around some theoretical simplifications, such as additive effects of mutations as they accumulate in the germ line over time. Mutations (and genes in general) may have non-additive interactions, referred to as Antagonistic Epistasis (when 2 + 2 = 3) or Synergystic Epistasis (2 + 2 = 5). Work with mathematician Dr. Troy Day has revealed important changes in the predictions of the MA hypothesis for ageing when mutations can evolve with epistasis. Meanwhile, we have built upon a novel protocol in Drosophila, developed by former PhD students M. Mallet and C. Kimber and current PhD I. Sayyed, to accumulate new mutations across nearly the entire genome to test the effects of MA. In conjunction with the Drosophila LTEE, we have manipulated the force of natural selection with age to allow or exclude mutations with effects at particular ages.
Current Projects
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Mutation Accumulation, Epistasis & Ageing [Imran & Ronni]
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Mutation Accumulation and Development [Ronni & Alannah]
Drosophila Long Term Evolution Experiment (LTEE)
Fruit fly evolution experiments have played a central role in exploring phenomena as diverse as pesticide resistance and mate choice. Among these is the evolution of ageing and life-history. One classic experiment was started by Michael Rose in 1980, who bred flies for increasingly later and later ages of reproduction, demonstrating genetic tradeoffs (Antagonistic Pleiotropy) between early and late reproduction and a host of life-history and stress resistance traits. Adam Chippindale joined the Rose Lab as a PhD student, and descendants of these same lines are maintained at Queen’s today. This Drosophila LTEE is certainly among the longest and most highly replicated ever undertaken in an animal species, with five-fold replication and some populations approaching 1 500 generations of selection (see phylogeny figure). The selection regimes are very simple, with discrete-generations of different durations (9, 14 and 28d), allowing populations of 1 600 – 2 000 animals to be maintained each generation. With the replicated structure, the system is ideal for testing ideas about parallel and convergent evolution. Current projects making use of the LTEE include the evolution of ageing (see MA sections), reproductive isolation between populations, sex roles and sexual selection under demographic pressure, and the evolution of reproductive systems.
