No abstract

Summary1. The timing of tree flushing follows strong phenotypic and genetic clines across environmental gradients. It may be seen as an adaptive response to abiotic (escape of spring frost and maximizing growing season length) and biotic (escape of pest and disease) hazards. However, few studies have investigated jointly both types of hazards. 2. We assessed exposure to both abiotic (spring frost) and biotic (powdery mildew) hazards within and between sessile oak populations along elevation gradients, during the flushing period in several years. For each population and phenological phenotype (early-vs. late-flushing trees), we estimated safety margins, defined as the time period separating budburst from the hazard occurrence (spore emission, spring frost). 3. We observed that powdery mildew phenology (initiation of spore release in spring) was less responsive to the elevation gradient than oak phenology (budburst) and that it was not correlated with tree phenology within populations. The spring frost and disease safety margins varied considerably between oak populations as a function of elevation and within populations in relation to tree phenological phenotype. For both hazards, safety margins decreased significantly with increasing elevation. The safety margin for spring frost was mostly positive (i.e. escape), whereas the safety margin for powdery mildew was mostly negative (i.e. exposure), leading to infection. The abiotic and biotic hazards interact in opposite directions with phenology, especially at low elevations (< 500 m) where early flushing enabled trees to escape disease while late flushing provided a higher safety margin against late frost. 4. Synthesis. The observed patterns suggest that oak populations are better adapted to escape spring frost than pathogen exposure all along the elevation gradient. The combination of the biotic and abiotic selective pressures may have contributed to the maintenance of phenological diversity within low-elevation tree populations. As tree and pathogen respond differently to environmental cues, climate change is likely to affect the phenological (a)synchrony between host and parasite, both within and between populations.

No abstract

The evolutionary perspective of cancer (which origins and dynamics result from evolutionary processes) has gained significant international recognition over the past decade and generated a wave of enthusiasm among researchers. In this context, several authors proposed that insights into evolutionary and adaptation dynamics of cancers can be gained by studying the evolutionary strategies of organisms. Although this reasoning is fundamentally correct, in our opinion, it contains a potential risk of excessive adaptationism, potentially leading to the suggestion of complex adaptations that are unlikely to evolve among cancerous cells. For example, the ability of recognizing related conspecifics and adjusting accordingly behaviors as in certain free-living species appears unlikely in cancer. Indeed, despite their rapid evolutionary rate, malignant cells are under selective pressures for their altered lifestyle for only few decades. In addition, even though cancer cells can theoretically display highly sophisticated adaptive responses, it would be crucial to determine the frequency of their occurrence in patients with cancer, before therapeutic applications can be considered. Scientists who try to explain oncogenesis will need in the future to critically evaluate the metaphorical comparison of selective processes affecting cancerous cells with those affecting organisms. This approach seems essential for the applications of evolutionary biology to understand the origin of cancers, with prophylactic and therapeutic applications.

For an increasing number of biologists, cancer is viewed as a dynamic system governed by evolutionary and ecological principles. Throughout most of human history, cancer was an uncommon cause of death and it is generally accepted that common components of modern culture, including increased physiological stresses and caloric intake, favor cancer development. However, the precise mechanisms for this linkage are not well understood. Here, we examine the roles of ecological and physiological disturbances and resource availability on the emergence of cancer in multicellular organisms. We argue that proliferation of ‘profiteering phenotypes’ is often an emergent property of disturbed, resource-rich environments at all scales of biological organization. We review the evidence for this phenomenon, explore it within the context of malignancy, and discuss how this ecological framework may offer a theoretical background for novel strategies of cancer prevention. This work provides a compelling argument that the traditional separation between medicine and evolutionary ecology remains a fundamental limitation that needs to be overcome if complex processes, such as oncogenesis, are to be completely understood.

BackgroundCarcinogenesis affects not only humans but almost all metazoan species. Understanding the rules driving the occurrence of cancers in the wild is currently expected to provide crucial insights into identifying how some species may have evolved efficient cancer resistance mechanisms. Recently the absence of correlation across species between cancer prevalence and body size (coined as Peto’s paradox) has attracted a lot of attention. Indeed, the disparity between this null hypothesis, where every cell is assumed to have an identical probability to undergo malignant transformation, and empirical observations is particularly important to understand, due to the fact that it could facilitate the identification of animal species that are more resistant to carcinogenesis than expected. Moreover it would open up ways to identify the selective pressures that may be involved in cancer resistance. However, Peto’s paradox relies on several questionable assumptions, complicating the interpretation of the divergence between expected and observed cancer incidences.DiscussionsHere we review and challenge the different hypotheses on which this paradox relies on with the aim of identifying how this null hypothesis could be better estimated in order to provide a standard protocol to study the deviation between theoretical/theoretically predicted and observed cancer incidence. We show that due to the disproportion and restricted nature of available data on animal cancers, applying Peto’s hypotheses at species level could result in erroneous conclusions, and actually assume the existence of a paradox. Instead of using species level comparisons, we propose an organ level approach to be a more accurate test of Peto’s assumptions.SummaryThe accuracy of Peto’s paradox assumptions are rarely valid and/or quantifiable, suggesting the need to reconsider the use of Peto’s paradox as a null hypothesis in identifying the influence of natural selection on cancer resistance mechanisms.

Hosts manipulated by parasites are profoundly altered organisms exhibiting a broad range of potential modifications. Exploring this multidimensionality is an emerging field. Previous studies have shown that the bird trematode Microphallus papillorobustus induces several behavioral changes in the gammarid Gammarus insensibilis. Knowing that aggregation behavior and reduced activity levels are strategies that limit predation in other species of amphipods, we explored in this study these behavioral responses for infected and uninfected G. insensibilis in the presence of host and non-host predator olfactory cues (bird feces and fish mucus). While uninfected individuals reduced their activity level in the presence of predator cues, infected individuals did not change their activity level in presence of aquatic bird feces. We also studied the gammarid aggregation behavior. Uninfected gammarids in clean water spent significantly more time in aggregates than did infected individuals. Among the uninfected individuals, the aggregation level tended to increase when bird feces and fish mucus were added, but the difference was not significant. Among infected individuals, the level of aggregation was significantly increased only with the bird feces. We discussed our results in the context of the literature on multidimensional manipulations, acknowledging that subtle differences between unparasitized and parasitized gammarids can also be by-products of manipulation on other traits.