Evolution determines how global warming and pesticide exposure will shape predator‐prey interactions with vector mosquitoes

How evolution may mitigate the effects of global warming and pesticide exposure on predator–prey interactions is directly relevant for vector control. Using a space‐for‐time substitution approach, we addressed how 4°C warming and exposure to the pesticide endosulfan shape the predation on Culex pipiens mosquitoes by damselfly predators from replicated low‐ and high‐latitude populations. Although warming was only lethal for the mosquitoes, it reduced predation rates on these prey. Possibly, under warming escape speeds of the mosquitoes increased more than the attack efficiency of the predators. Endosulfan imposed mortality and induced behavioral changes (including increased filtering and thrashing and a positional shift away from the bottom) in mosquito larvae. Although the pesticide was only lethal for the mosquitoes, it reduced predation rates by the low‐latitude predators. This can be explained by the combination of the evolution of a faster life history and associated higher vulnerabilities to the pesticide (in terms of growth rate and lowered foraging activity) in the low‐latitude predators and pesticide‐induced survival selection in the mosquitoes. Our results suggest that predation rates on mosquitoes at the high latitude will be reduced under warming unless predators evolve toward the current low‐latitude phenotype or low‐latitude predators move poleward

An integrated multi-omics approach identifies the landscape of interferon-α-mediated responses of human pancreatic beta cells

Interferon-α (IFNα), a type I interferon, is expressed in the islets of type 1 diabetic individuals, and its expression and signaling are regulated by T1D genetic risk variants and viral infections associated with T1D. We presently characterize human beta cell responses to IFNα by combining ATAC-seq, RNA-seq and proteomics assays. The initial response to IFNα is characterized by chromatin remodeling, followed by changes in transcriptional and translational regulation. IFNα induces changes in alternative splicing (AS) and first exon usage, increasing the diversity of transcripts expressed by the beta cells. This, combined with changes observed on protein modification/degradation, ER stress and MHC class I, may expand antigens presented by beta cells to the immune system. Beta cells also up-regulate the checkpoint proteins PDL1 and HLA-E that may exert a protective role against the autoimmune assault. Data mining of the present multi-omics analysis identifies two compound classes that antagonize IFNα effects on human beta cells.This article is freely available via Open Access. Click on the Publisher URL to access it via the publisher's site.P30 DK097512/DK/NIDDK NIH HHS/United States UC4 DK104166/DK/NIDDK NIH HHS/United States MR/P010695/1/MRC_/Medical Research Council/United Kingdompublished version, accepted version, submitted versio

Molecular regulation of auditory hair cell death and approaches to protect sensory receptor cells and/or stimulate repair following acoustic trauma

International audienceLoss of auditory sensory hair cells (HCs) is the most common cause of hearing loss. This review addresses the signaling pathways that are involved in the programmed and necrotic cell death of auditory HCs that occur in response to ototoxic and traumatic stressor events. The roles of inflammatory processes, oxidative stress, mitochondrial damage, cell death receptors, members of the mitogen-activated protein kinase (MAPK) signal pathway and pro- and anti-cell death members of the Bcl-2 family are explored. The molecular interaction of these signal pathways that initiates the loss of auditory HCs following acoustic trauma is covered and possible therapeutic interventions that may protect these sensory HCs from loss via apoptotic or non-apoptotic cell death are explored

Mechanisms of viral entry: sneaking in the front door

Recent developments in methods to study virus internalisation are providing clearer insights into mechanisms used by viruses to enter host cells. The use of dominant negative constructs, specific inhibitory drugs and RNAi to selectively prevent entry through particular pathways has provided evidence for the clathrin-mediated entry of hepatitis C virus (HCV) as well as the caveolar entry of Simian Virus 40. Moreover, the ability to image and track fluorescent-labelled virus particles in real-time has begun to challenge the classical plasma membrane entry mechanisms described for poliovirus and human immunodeficiency virus. This review will cover both well-documented entry mechanisms as well as more recent discoveries in the entry pathways of enveloped and non-enveloped viruses. This will include viruses which enter the cytosol directly at the plasma membrane and those which enter via endocytosis and traversal of internal membrane barrier(s). Recent developments in imaging and inhibition of entry pathways have provided insights into the ill-defined entry mechanism of HCV, bringing it to the forefront of viral entry research. Finally, as high-affinity receptors often define viral internalisation pathways, and tropism in vivo, host membrane proteins to which viral particles specifically bind will be discussed throughout

The interplay between pesticides and biotic interactions in damselflies under global warming

Two major challenges for population persistence are global warming and the exposure to chemical pesticides. Both challenges are directly linked since both the use of pesticides and their toxicity is expected to increase under warming. In my PhD, I integrate the effects of temperature and pesticide stress on different levels of biological organization going from the (sub)organismal level up to the level of performance traits (thermal tolerance), biotic interactions (mainly competition) and ecosystem functions. My focal species is the damselfly Ischnura elegans, where I not only study plastic effects of exposure to higher temperatures but also evaluate the role of gradual thermal evolution and potential feedback loops to pesticide vulnerability by using a space-for-time substitution approach. To address these issues I combine laboratory common garden warming experiments with outdoor heated mesocosm experiments where I simulate global warming scenarios.status: publishe

Data Op de Beeck et al. 2017JAPPL

Excel file with data on life history (mortality and growth) and physiology of the damselfly Ischnura elegans as a response to the pesticide chlorpyrifos, warming and latitude

Stoichiometric responses to an agricultural pesticide are modified by predator cues

Current ecological risk assessment of pesticides fails to protect aquatic ecosystem health. To get better insight in how pesticides may affect aquatic ecosystems, we tested how sublethal pesticide concentrations modify body stoichiometry. Moreover, as interactions with natural stressors may cause underestimates of the impact of pesticides, we also tested whether this pathway depended on the presence of predator cues. Therefore, we exposed damselfly larvae to chlorpyrifos and cues from predatory dragonflies and focused on body stoichiometry and associated explanatory variables (growth rate, RNA:DNA and energy storage molecules). The way the predator cues modulated the pesticide effects strongly differed between endpoints. Exposure to chlorpyrifos affected the key body stoichiometric ratios: chlorpyrifos consistently increased N:P, while its effects on C:N (decrease with predator cues) and C:P (increase without predator cues) strongly depended upon the presence of the natural stressor. These stoichiometric responses could be explained by associated changes in growth, RNA:DNA and in C-rich fat and sugars and N-rich proteins. The observed changes in body stoichiometry may affect the damselflies’ food quality, and have the potential to cascade through the food web and shape nutrient cycling.status: publishe

Competition magnifies the impact of a pesticide in a warming world by reducing heat tolerance and increasing autotomy

There is increasing concern that standard laboratory toxicity tests may be misleading when assessing the impact of toxicants, because they lack ecological realism. Both warming and biotic interactions have been identified to magnify the effects of toxicants. Moreover, while biotic interactions may change the impact of toxicants, toxicants may also change the impact of biotic interactions. However, studies looking at the impact of biotic interactions on the toxicity of pesticides and vice versa under warming are very scarce. Therefore, we tested how warming (+4 °C), intraspecific competition (density treatment) and exposure to the pesticide chlorpyrifos, both in isolation and in combination, affected mortality, cannibalism, growth and heat tolerance of low- and high-latitude populations of the damselfly Ischnura elegans. Moreover, we addressed whether toxicant exposure, potentially in interaction with competition and warming, increased the frequency of autotomy, a widespread antipredator mechanism. Competition increased the toxicity of chlorpyrifos and made it become lethal. Cannibalism was not affected by chlorpyrifos but increased at high density and under warming. Chlorpyrifos reduced heat tolerance but only when competition was high. This is the first demonstration that a biotic interaction can be a major determinant of 'toxicant-induced climate change sensitivity'. Competition enhanced the impact of chlorpyrifos under warming for high-latitude larvae, leading to an increase in autotomy which reduces fitness in the long term. This points to a novel pathway how transient pesticide pulses may cause delayed effects on populations in a warming world. Our results highlight that the interplay between biotic interactions and toxicants have a strong relevance for ecological risk assessment in a warming polluted world.status: publishe