Professor Stuart West
Professor of Evolutionary Biology
My pronouns are he/him
I am an evolutionary biologist whose main interest is adaptation, and especially the evolution of social behaviours, such as cooperation, altruism, spite, mutualism, and how these can influence major evolutionary transitions. I use a mixture of techniques including theory, experiment and across species comparative studies.
Our current work is focused on the evolution of cooperation and division of labour, with a mixture of: genomic analyses (mainly bacteria); across species comparative studies (mainly insects); theoretical modelling; and experiments (mainly bacteria). See Publications for recent examples.
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Bacterial death is critical in nutrient recycling. However, the underlying mechanisms that permit macromolecule recycling after bacterial death are largely unknown. We demonstrate that bacteria encode post-mortem protein catabolism via Lon protease released from the dead bacteria. Growth assays reveal that the lysate of Lon protease-null bacteria does not provide a growth benefit to wild type cells. This deficiency is reversed with exogenous recombinant Lon protease, confirming its post-mortem role and is independent of Lon ATPase activity. Biochemistry, growth assays and metabolomics demonstrate that Lon protease facilitates peptide nutrient release, benefitting living cells and acting as a cooperative public good. We also show that the production of Lon protease cannot be explained by a personal benefit to living cells. Although Lon protease can also provide a benefit to living cells under stressful conditions by helping control protein quality, this private benefit does not outweigh the cost under the conditions examined. These results suggest that Lon protease represents a post-mortem adaptation that can potentially be explained by considering the post-mortem indirect benefit to other cells (kin selection). This discovery highlights an unexpected post-mortem biochemistry, reshaping our understanding of nutrient recycling.
Experiments have shown that when one plant is attacked by a pathogen or herbivore, this can lead to other plants connected to the same mycorrhizal network up-regulating their defense mechanisms. It has been hypothesized that this represents signaling, with attacked plants producing a signal to warn other plants of impending harm. We examined the evolutionary plausibility of this and other hypotheses theoretically. We found that the evolution of plant signaling about an attack requires restrictive conditions, and so will rarely be evolutionarily stable. The problem is that signaling about an attack provides a benefit to competing neighbors, even if they are kin, and so reduces the relative fitness of signaling plants. Indeed, selection is often more likely to push plant behavior in the opposite direction—with plants signaling dishonestly about an attack that has not occurred, or suppressing a cue that they have been attacked. Instead, we show that there are two viable alternatives that could explain the empirical data: 1) the process of being attacked leads to a cue (information about the attack) which is too costly for the attacked plant to fully suppress; 2) mycorrhizal fungi monitor their host plants, detect when they are attacked, and then the fungi signal this information to warn other plants in their network. Our results suggest the empirical work that would be required to distinguish between these possibilities.
signaling
,cooperation
,plant-fungal networks
,evolutionary theory
,social evolution
Comparative genomics, whereby the genomes of different species are compared, has the potential to address broad and fundamental questions at the intersection of genetics and evolution. However, species, genomes and genes cannot be considered as independent data points within statistical tests. Closely related species tend to be similar because they share genes by common descent, which must be accounted for in analyses. This problem of non-independence may be exacerbated when examining genomes or genes but can be addressed by applying phylogeny-based methods to comparative genomic analyses. Here, we review how controlling for phylogeny can change the conclusions of comparative genomics studies. We address common questions on how to apply these methods and illustrate how they can be used to test causal hypotheses. The combination of rapidly expanding genomic datasets and phylogenetic comparative methods is set to revolutionize the biological insights possible from comparative genomic studies.
This chapter studies strategic behavior when agents have no information about the structure of the underlying game and they cannot observe other agents' actions or payoffs. Even when players have no such information, there are simple payoff-based learning rules that lead to Nash equilibrium in many types of games, as shown in Chapter 8. A key feature of these trial-and-error rules is that subjects search differently depending on whether their payoffs increase, stay constant, or decrease. This chapter analyzes learning behavior in a laboratory setting and finds strong empirical confirmation for these asymmetric search behaviors in the context of voluntary contribution games. By varying the amount of information, we show that these behaviors are also present even when subjects have full information about the game.
38 Economics
,3803 Economic Theory
3107 Microbiology
,31 Biological Sciences
,3104 Evolutionary Biology
Hamilton's rule provides the cornerstone for our understanding of the evolution of all forms of social behavior, from altruism to spite, across all organisms, from viruses to humans. In contrast to the standard prediction from Hamilton's rule, recent studies have suggested that altruistic helping can be favored even if it does not benefit relatives, as long as it decreases the environmentally induced variance of their reproductive success ("altruistic bet-hedging"). However, previous predictions both rely on an approximation and focus on variance-reducing helping behaviors. We derived a version of Hamilton's rule that fully captures environmental variability. This shows that decreasing (or increasing) the variance in the absolute reproductive success of relatives does not have a consistent effect-it can either favor or disfavor the evolution of helping. We then empirically quantified the effect of helping on the variance in reproductive success across 15 species of cooperatively breeding birds. We found that a) helping did not consistently decrease the variance of reproductive success and often increased it, and b) the mean benefits of helping across environments consistently outweighed other variability components of reproductive success. Altogether, our theoretical and empirical results suggest that the effects of helping on the variability components of reproductive success have not played a consistent or strong role in favoring helping.
kin selection
,bet- hedging
,cooperative breeding
,social evolution
<jats:title>Abstract</jats:title><jats:p>The size–complexity hypothesis is a leading explanation for the evolution of complex life on earth. It predicts that in lineages that have undergone a major transition in organismality, larger numbers of lower-level subunits select for increased division of labour. Current data from multicellular organisms and social insects support a positive correlation between the number of cells and number of cell types and between colony size and the number of castes. However, the implication of these results is unclear, because colony size and number of cells are correlated with other variables which may also influence selection for division of labour, and causality could be in either direction. Here, to resolve this problem, we tested multiple causal hypotheses using data from 794 ant species. We found that larger colony sizes favoured the evolution of increased division of labour, resulting in more worker castes and greater variation in worker size. By contrast, our results did not provide consistent support for alternative hypotheses regarding either queen mating frequency or number of queens per colony explaining variation in division of labour. Overall, our results provide strong support for the size–complexity hypothesis.</jats:p>
E: | stuart.west@biology.ox.ac.uk |
T: | 01865 (2) 81998 |
X: @StuWest8 | |
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