Extensive individual variation in spatial behaviour is a common feature among species that exhibit migratory life cycles. Nowhere is this more evident than in salmonid fishes; individual fish may complete their entire life cycle in freshwater streams, others may migrate variable distances at sea and yet others limit their migrations to larger rivers or lakes before returning to freshwater streams to spawn. This review presents evidence that individual variation in migratory behaviour and physiology in salmonid fishes is controlled by developmental thresholds and that part of the variation in proximal traits activating the development of alternative migratory tactics is genetically based. We summarize evidence that alternative migratory tactics co-exist within populations and that all individuals may potentially adopt any of the alternative phenotypes. Even though intra-specific genetic divergence of migratory tactics is uncommon, it may occur if female competition for oviposition sites results in spawning segregation of alternative phenotypes. Because of their polygenic nature, alternative migratory tactics are considered as threshold traits. Threshold traits have two characteristics: an underlying 'liability' trait that varies in a continuous fashion, and a threshold value which is responsible for the discreetness observed in phenotypic distribution. We review evidence demonstrating that body size is an adequate proxy for the liability trait controlling the decision to migrate, but that the same phenotypic outcome (anadromy or residency) may be reached by different developmental pathways. The evidence suggesting a significant heritable component in the development of alternative migratory tactics is subsequently reviewed, leading us to conclude that alternative migratory tactics have considerable potential to respond to selection and evolve. We review what is known about the proximal physiological mechanisms mediating the translation of the continuous value of the liability trait into a discontinuous migratory tactic. We conclude by identifying several avenues for future research, including testing the frequency-dependent selection hypothesis, establishing the relative importance of adaptive phenotypic plasticity in explaining some geographic gradients in migratory behaviour and identifying the physiological and genetic basis of the switching mechanisms responsible for alternative migratory tactics.

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SUMMARY Understanding infection dynamics in animal hosts is fundamental to managing spillover and emergence of zoonotic infections. Hendra virus is endemic in Australian pteropodid bat populations and can be lethal to horses and humans. However, we know little about the factors driving Hendra virus prevalence in resevoir bat populations, making spillover difficult to predict. We use Hendra virus prevalence data collected from 13 000 pooled bat urine samples across space and time to determine if pulses of prevalence are periodic and synchronized across sites. We also test whether site-specific precipitation and temperature affect the amplitude of the largest annual prevalence pulses. We found little evidence for a periodic signal in Hendra virus prevalence. Although the largest amplitude pulses tended to occur over winter, pulses could also occur in other seasons. We found that Hendra virus prevalence was weakly synchronized across sites over short distances, suggesting that prevalence is driven by local-scale effects. Finally, we found that drier conditions in previous seasons and the abundance of Pteropus alecto were positively correlated with the peak annual values of Hendra virus prevalence. Our results suggest that in addition to seasonal effects, bat density and local climatic conditions interact to drive Hendra virus infection dynamics.

Superspreading, the phenomenon where a small proportion of individuals contribute disproportionately to new infections, has profound effects on disease dynamics. Superspreading can arise through variation in contacts, infectiousness or infectious periods. The latter has received little attention, yet it drives the dynamics of many diseases of critical public health, livestock health and conservation concern. Here, we present rare evidence of variation in infectious periods underlying a superspreading phenomenon in a free-ranging wildlife system. We detected persistent infections of Mycoplasma ovipneumoniae, the primary causative agent of pneumonia in bighorn sheep (Ovis canadensis), in a small number of older individuals that were homozygous at an immunologically relevant genetic locus. Interactions among age-structure, genetic composition and infectious periods may drive feedbacks in disease dynamics that determine the magnitude of population response to infection. Accordingly, variation in initial conditions may explain divergent population responses to infection that range from recovery to catastrophic decline and extirpation.

Hosts have evolved two distinct defence strategies against parasites: resistance (which prevents infection or limit parasite growth) and tolerance (which alleviates the fitness consequences of infection). However, heritable variation in resistance and tolerance and the genetic correlation between these two traits have rarely been characterized in wild host populations. Here, we estimate these parameters for both traits in Leuciscus burdigalensis, a freshwater fish parasitized by Tracheliastes polycolpus. We used a genetic database to construct a full-sib pedigree in a wild L. burdigalensis population. We then used univariate animal models to estimate inclusive heritability (i.e. all forms of genetic and non-genetic inheritance) in resistance and tolerance. Finally, we assessed the genetic correlation between these two traits using a bivariate animal model. We found significant heritability for resistance (H ¼ 17.6%; 95% CI: 7.2-32.2%) and tolerance (H ¼ 18.8%; 95% CI: 4.4-36.1%), whereas we found no evidence for the existence of a genetic correlation between these traits. Furthermore, we confirm that resistance and tolerance are strongly affected by environmental effects. Our results demonstrate that (i) heritable variation exists for parasite resistance and tolerance in wild host populations, and (ii) these traits can evolve independently in populations.

Abstract:Modern weed science is at a crossroads. Born out of advances in chemistry, it has focused on minimizing weed competition with genetically uniform crops and heavy reliance on herbicides. Paradoxically, the success obtained with such an approach and the reluctance to conduct integrated and multidisciplinary research has resulted in unintended, but predictable, consequences, including the selection of herbicide resistant biotypes. Advances in eco-evolutionary biology, a relatively recent discipline that seeks to understand how local population dynamics arise from phenotypic variation resulting from natural selection, habitat distribution, and propagule dispersal across the landscape are transforming our understanding of the processes that regulate agroecosystems. Within this framework, complementary tactics to develop alternative weed management programs include the following: (1) weed scientists must recognize that evolution occurs within crop fields at ecologically-relevant time scales and is rooted in the inherent variation that exists in all populations; (2) weed management should recognize that the probability of a resistant mutant is directly related to the population size; (3) farmers need to acknowledge that herbicide resistance transcends any one farm and should coordinate local practices with regional actions; (4) incentives should be developed and implemented to help the adoption of eco-evolutionary management programs; and (5) risk analysis can help incorporate an eco-evolutionary perspective into integrated weed management programs.

Migratory behaviour with its associated phenotypic changes is generally viewed as an adaptive strategy because it incurs survival or reproductive advantages to migrants. The development of a migrant phenotype is believed to be controlled by threshold mechanisms, where individuals emigrate only after surpassing a particular body size but delay migration if below. For such a strategy to respond to natural selection, part of the phenotypic variance in the propensity to migrate must be explained by variation in additive genetic effects. Here, we use data gathered in the field and from a common rearing experiment to test for a genetic basis associated with seaward migration in Atlantic salmon (Salmo salar L.). We document a high heritability of the liability trait underlying the propensity to emigrate in juvenile salmon, and significant differences between offspring grouped according to their sires in body‐size threshold values above which emigration takes place. The presence of additive genetic variance in both the liability and thresholds makes the onset of migration a process sensitive to selection and may therefore constitute an important explanatory mechanism for the interpopulation differences in the size at seaward migration observed in this species.

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