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Novel behaviours can spur evolutionary change and sometimes even precede morphological innovation, but the evolutionary and developmental contexts for their origins can be elusive. One proposed mechanism to generate behavioural innovation is a shift in the developmental timing of gene-expression patterns underlying an ancestral behaviour, or molecular heterochrony. Alternatively, novel suites of gene expression, which could provide new contexts for signalling pathways with conserved behavioural functions, could promote novel behavioural variation. To determine the relative contributions of these alternatives to behavioural innovation, I used a species of spadefoot toad, Spea bombifrons. Based on environmental cues, Spea larvae develop as either of two morphs 'omnivores' that, like their ancestors, feed on detritus, or 'carnivores' that are predaceous and cannibalistic. Because all anuran larvae undergo a natural transition to obligate carnivory during metamorphosis, it has been proposed that the novel, predaceous behaviour in Spea larvae represents the accelerated activation of gene networks influencing post-metamorphic behaviours. Based on comparisons of brain transcriptional profiles, my results reject widespread heterochrony as a mechanism promoting the expression of predaceous larval behaviour. They instead suggest that the evolution of this trait relied on novel patterns of gene expression that include components of pathways with conserved behavioural functions.Traditionally, resistance and resilience are associated with good ecological health, often underpinning restoration goals. However, degraded ecosystems can also be highly resistant and resilient, making restoration difficult degraded communities often become dominated by hyper-tolerant species, preventing recolonization and resulting in low biodiversity and poor ecosystem function. Using streams as a model, we undertook a mesocosm experiment to test if degraded community presence hindered biological recovery. We established 12 mesocosms, simulating physically healthy streams. Degraded invertebrate communities were established in half, mimicking the post-restoration scenario of physical recovery without biological recovery. We then introduced a healthy colonist community to all mesocosms, testing if degraded community presence influenced healthy community establishment. Colonists established less readily in degraded community mesocosms, with larger decreases in abundance of sensitive taxa, likely driven by biotic interactions rather than abiotic constraints. Resource depletion by the degraded community likely increased competition, driving priority effects. Colonists left by drifting, but also by accelerating development, reducing time to emergence but sacrificing larger body size. Since degraded community presence prevented colonist establishment, our experiment suggests successful restoration must address both abiotic and biotic factors, especially those that reinforce the 'negative' resistance and resilience which perpetuate degraded communities and are typically overlooked.Predation traces found on fossilized prey remains can be used to quantify the evolutionary history of biotic interactions. Fossil mollusc shells bearing these types of traces provided key evidence for the rise of predation during the Mesozoic marine revolution (MMR), an event thought to have reorganized global marine ecosystems. However, predation pressure on prey groups other than molluscs has not been explored adequately. Consequently, the ubiquity, tempo and synchronicity of the MMR cannot be thoroughly assessed. Here, we expand the evolutionary record of biotic interactions by compiling and analysing a new comprehensively collected database on drilling predation in Meso-Cenozoic echinoids. Trends in drilling frequency reveal an Eocene rise in drilling predation that postdated echinoid infaunalization and the rise in mollusc-targeted drilling (an iconic MMR event) by approximately 100 Myr. The temporal lag between echinoid infaunalization and the rise in drilling frequencies suggests that the Eocene upsurge in predation did not elicit a coevolutionary or escalatory response. This is consistent with rarity of fossil samples that record high frequency of drilling predation and scarcity of fossil prey recording failed predation events. These results suggest that predation intensification associated with the MMR was asynchronous across marine invertebrate taxa and represented a long and complex process that consisted of multiple uncoordinated steps probably with variable coevolutionary responses.Numerous threats are putting pollinator health and essential ecosystem pollination services in jeopardy. Although individual threats are widely studied, their co-occurrence may exacerbate negative effects, as posited by the multiple stressor hypothesis. CDDO-Im activator A prominent branch of this hypothesis concerns pesticide-pathogen co-exposure. A landscape analysis demonstrated a positive association between local chlorothalonil fungicide use and microsporidian pathogen (Nosema bombi) prevalence in declining bumblebee species (Bombus spp.), suggesting an interaction deserving further investigation. We tested the multiple stressor hypothesis with field-realistic chlorothalonil and N. bombi exposures in worker-produced B. impatiens microcolonies. Chlorothalonil was not avoided in preference assays, setting the stage for pesticide-pathogen co-exposure. However, contrary to the multiple stressor hypothesis, co-exposure did not affect survival. Bees showed surprising tolerance to Nosema infection, which was also unaffected by chlorothalonil exposure. However, previously fungicide-exposed infected bees carried more transmission-ready spores. Our use of a non-declining bumblebee and potential higher chlorothalonil exposures under some scenarios could mean stronger individual or interactive effects in certain field settings. Yet, our results alone suggest consequences of pesticide co-exposure for pathogen dynamics in host communities. This underlies the importance of considering both within- and between-host processes when addressing the multiple stressor hypothesis in relation to pathogens.

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