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Search indexed bioRxiv preprints in genomics, neuroscience, cell biology and bioinformatics. Read source abstracts and check manuscript versions; preprints are not peer reviewed.

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bioRxiv2018

Data-driven modeling of cholinergic modulation of neural microcircuits: bridging neurons, synapses, and network states

1Neuromodulators, such as acetylcholine (ACh), control information processing in neural microcircuits by regulating neuronal and synaptic physiology. Computational models and simulations enable predictions on the potential role of ACh in reconfiguring network states. As a prelude into investigating how the cellular and synaptic effects of ACh collectively influence emergent network dynamics, we developed a data-driven framework incorporating phenomenological models of the anatomy and physiology of cholinergic modulation of the neocortex. The first-draft models were integrated into a biologically detailed tissue model of neocortical microcircuitry to predict how ACh affects different types of neurons and synapses, and consequently alters global network states. Preliminary simulations not only corroborate the long-standing notion that ACh desynchronizes network activity, but also reveal a potentially finegrained control over a spectrum of neocortical states. We show that low levels of ACh, such as those during sleep, drive microcircuit activity into slow oscillations and network synchrony, whereas high ACh concentrations, such as those during wakefulness, govern fast oscillations and network asynchrony. In addition, network states modulated by ACh levels shape spike-time cross-correlations across distinct neuronal populations in strikingly different ways. These effects are likely due to the differential regulation of neurons and synapses caused by increasing levels of ACh that enhances cellular excitability by increasing neuronal activity and decreases the efficacy of local synaptic transmission by altering neurotransmitter release probability. We conclude by discussing future directions to refine the biological accuracy of the framework, which will extend its utility and foster the development of hypotheses to investigate the role of neuromodulation in neural information processing.

neuroscience↗

bioRxiv2018

Glutathione shapes glutamatergic transmission

Glutamate is the most abundant excitatory neurotransmitter, present at the bulk of cortical synapses, and participating in many physiologic and pathologic processes ranging from learning and memory to stroke. The tripeptide, glutathione, is one third glutamate and present at up to low millimolar intracellular concentrations in brain, mediating antioxidant defenses and drug detoxification. Because of the substantial amounts of brain glutathione and its rapid turnover under homeostatic control, we hypothesized that glutathione is a relevant reservoir of glutamate, and could influence synaptic excitability. We find that drugs which inhibit generation of glutamate by the glutathione cycle elicit decreases in cytosolic glutamate and decreased miniature excitatory post synaptic potential (mEPSC) frequency. In contrast, pharmacologically decreasing the biosynthesis of glutathione leads to increases in cytosolic glutamate and enhanced mEPSC frequency. The glutathione cycle can compensate for decreased excitatory neurotransmission when the glutamate-glutamine shuttle is inhibited. Glutathione may be a physiologic reservoir of glutamate neurotransmitter.\n\nSignificanceGlutathione is the principal antioxidant and redox regulator in cells. In addition to its essential roles in redox homeostasis it functions as cofactors for a multitude of enzymes. We show here that glutathione is a reservoir for synaptic glutamate, the excitatory neurotransmitter in the central nervous system. Deficits in glutathione have been linked to multiple neurodegenerative and neuropsychiatric disorders. Accordingly, agents that restore glutathione-glutamate homeostasis may afford therapeutic benefit.

neuroscience↗

bioRxiv2018

Body size-dependent energy storage causes Kleibers law scaling of the metabolic rate in planarians

Kleibers law, or the [3/4]-power law scaling of the metabolic rate with body mass, is considered one of the few quantitative laws in biology, yet its physiological basis remains unknown. Here, we report Kleibers law scaling in the planarian Schmidtea mediterranea. Its reversible and life history-independent changes in adult body size over 2 orders of magnitude reveal that Kleibers law does not emerge from the size-dependent decrease in cellular metabolic rate, but from a size-dependent increase in mass per cell. Through a combination of experiment and theoretical analysis of the organismal energy balance, we further show that the mass allometry is caused by body size dependent energy storage. Our results reveal the physiological origins of Kleibers law in planarians and thus have general implications for understanding a fundamental scaling law in biology.

biophysics↗

bioRxiv2018

The maternal hormone in the male brain: sexually dimorphic distribution of prolactin signalling in the mouse brain

Research of the central actions of prolactin is virtually restricted to females, but this hormone has also documented roles in male physiology and behaviour. Here, we provide the first description of the pattern of prolactin-derived signalling in the male mouse brain, employing the immunostaining of phosphorylated signal transducer and activator of transcription 5 (pSTAT5) after exogenous prolactin administration. Next, we explore possible sexually dimorphic differences by comparing pSTAT5 immunoreactivity in prolactin-supplemented males and females. We also assess the role of testosterone in the regulation of central prolactin signalling in males by comparing intact with castrated prolactin-supplemented males.\n\nProlactin-supplemented males displayed a widespread pattern of pSTAT5 immunoreactivity, restricted to brain centres showing expression of the prolactin receptor. Immunoreactivity for pSTAT5 was present in several nuclei of the preoptic, anterior and tuberal hypothalamus, as well as in the septofimbrial nucleus or posterodorsal medial amygdala of the telencephalon. Conversely, non-supplemented control males were virtually devoid of pSTAT5-immunoreactivity, suggesting that central prolactin actions in males are limited to situations concurrent with substantial hypophyseal prolactin release (e.g. stress or mating). Furthermore, comparison of prolactin-supplemented males and females revealed a significant, female-biased sexual dimorphism, supporting the view that prolactin has a preeminent role in female physiology and behaviour. Finally, in males, castration significantly reduced pSTAT5 immunoreactivity in some structures, including the paraventricular and ventromedial hypothalamic nuclei and the septofimbrial region, thus indicating a region-specific regulatory role of testosterone over central prolactin signalling.

neuroscience↗

bioRxiv2018

Transmembrane Protein 135 (TMEM135) is a Liver X Receptor Target Gene that Mediates an Auxiliary Peroxisome Matrix Protein Import Pathway

The liver x receptors (LXRs) are key regulators of systemic lipid metabolism. We determined whether transmembrane protein 135 (TMEM135) is an LXR target gene and its physiologic function. An LXR agonist increased TMEM135 mRNA and protein in human hepatocyte and macrophage cell lines, which was prevented by LXR knockdown. The human TMEM135 promoter contains an LXR response element that bound the LXRs via EMSA and ChIP, and mediated LXR-induced transcription in reporter assays. Knockdown of TMEM135 in HepG2 cells caused triglyceride accumulation despite reduced lipogenic gene expression, indicating a potential role in {beta}-oxidation. To determine physiologic importance, TMEM135 was knocked-down via siRNA in livers of fed and fasted C57BL/6 mice. Fasting increased hepatic fatty acid and NADH concentrations in control mice, consistent with increased fatty acid uptake and {beta}-oxidation. However, in fasted TMEM135 knockdown mice, there was a further significant increase in hepatic fatty acid concentrations and a significant decrease in NADH, indicating an impairment in {beta}-oxidation by peroxisomes and/or mitochondria. Conversely, hepatic ketones tended to increase in fasted TMEM135 knockdown compared to control mice, and because ketogenesis is exclusively dependent on mitochondrial {beta}-oxidation, this indicates peroxisomal {beta}-oxidation was impaired in knockdown mice. Localization studies demonstrated that TMEM135 co-localized with peroxisomes but not mitochondria. Mechanistically, proteomic and Western blot analyses indicated that TMEM135 regulates concentrations of matrix enzymes within peroxisomes. In conclusion, TMEM135 is a novel LXR target gene in humans that mediates peroxisomal metabolism, and thus TMEM135 may be a therapeutic target for metabolic disorders associated with peroxisome dysfunction.

cell biology↗

bioRxiv2018

Arabidopsis species deploy distinct strategies to cope with drought stress

O_LIBackground and Aims Water limitation is an important determinant of the distribution, abundance and diversity of plant species. Yet, little is known about how the response to limiting water supply changes among closely related plant species with distinct ecological preferences. Comparison of the model annual species A. thaliana to its close perennial relatives A. lyrata and A. halleri, can help disentangle the molecular and physiological changes contributing to tolerance and avoidance mechanisms, because these species must maintain tolerance and avoidance mechanisms to increase long-term survival, but they are exposed to different levels of water stress and competition in their natural habitat.\nC_LIO_LIMethods We conducted a dry-down experiment that mimics a period of missing precipitation. We quantified the covariation of progressive decrease in soil water content (SWC) with various physiological and morphological plant traits across a set of representative genotypes in Arabidopsis thaliana, A. lyrata and A. halleri. To quantify the degree of plant stress, transcriptome changes were also monitored.\nC_LIO_LIKey Results The analysis of trait co-variation demonstrates that the three species differ in the strategies they deploy to respond to drought stress. A. thaliana showed drought avoidance reaction but failed to survive wilting. A. lyrata efficiently combined avoidance and tolerance mechanisms. By contrast, A. halleri showed some degree of tolerance to wilting but it did not seem to protect itself from the stress imposed by drought. Transcriptome data collected just before plant wilting and after recovery corroborated the phenotypic analysis, with A. lyrata and A. halleri showing a stronger activation of recovery- and stress-related genes, respectively.\nC_LIO_LIConclusions We conclude that these three Arabidopsis species have evolved distinct strategies to face drought stress, and discuss the extent to which these strategic differences reflect their respective ecological priorities.\nC_LI

plant biology↗

bioRxiv2018

Measuring narrative engagement: The heart tells the story

Stories play a fundamental role in human culture. They provide a mechanism for sharing cultural identity, imparting knowledge, revealing beliefs, reinforcing social bonds and providing entertainment that is central to all human societies. Here we investigated the extent to which the delivery medium of a story (audio or visual) affected conscious and subconscious engagement with the narrative. Although participants self-reported greater involvement for watching video relative to listening to auditory scenes, stronger physiological responses were recorded for auditory stories. Sensors placed at their wrists showed higher and more variable heart rates, greater electrodermal activity, and even higher body temperatures. We interpret these findings as physiological evidence that the stories were more cognitively and emotionally engaging when presented in an auditory format. This may be because listening to a story, rather than watching a video, is a more active process of co-creation, and that this imaginative process in the listeners mind is detectable on the skin at their wrist.

neuroscience↗

bioRxiv2018

An atlas of protein-protein interactions across mammalian tissues

Cellular processes arise from the dynamic organization of proteins in networks of physical interactions. Mapping the complete network of biologically relevant protein-protein interactions, the interactome, has therefore been a central objective of high-throughput biology. Yet, because widely used methods for high-throughput interaction discovery rely on heterologous expression or genetically manipulated cell lines, the dynamics of protein interactions across physiological contexts are poorly understood. Here, we use a quantitative proteomic approach combining protein correlation profiling with stable isotope labelling of mammals (PCP SILAM) to map the interactomes of seven mouse tissues. The resulting maps provide the first proteome-scale survey of interactome dynamics across mammalian tissues, revealing over 27,000 unique interactions with an accuracy comparable to the highest-quality human screens. We identify systematic suppression of cross-talk between the evolutionarily ancient housekeeping interactome and younger, tissue-specific modules. Rewiring of protein interactions across tissues is widespread, and is poorly predicted by gene expression or coexpression. Rewired proteins are tightly regulated by multiple cellular mechanisms and implicated in disease. Our study opens up new avenues to uncover regulatory mechanisms that shape in vivo interactome responses to physiological and pathophysiological stimuli in mammalian systems.

systems biology↗

bioRxiv2018

A 14-day Dexamethasone timecourse exposure in Caco-2 monolayers results in differential expression of tight-junction and cytoskeleton regulatory pathway genes

Glucocorticoid (GC) hormones are modulators of endogenous stress responses and are important pharmaceuticals for inflammatory and autoimmune diseases. The gastrointestinal epithelium is a significant tissue target of Glucocorticoids; perturbation of epithelial barrier function during the endogenous stress response plays a major role in the pathophysiology of inflammatory bowel disease. Epithelial permeability and barrier function are mediated by the tight junction protein complex, with a network of molecular/cellular interactions occurring between the actin cytoskeleton, RhoGTPase, Akt/PI3K and growth factor receptor, and inflammatory cytokine signaling, influencing the establishment of a partial EMT phenotype. To improve our understanding of GC-responsive gene expression in a gastrointestinal epithelial context, we tested polarized Caco-2 monolayer cultures during at 30-day timecourse, with 15-days of continuous Dexamethasone exposure. Trans-epithelial resistance (TEER) was recorded to provide a physiological quantification of barrier function during the timecourse treatments. Presence of intracellular glucocorticoid hormone activates the human glucocorticoid receptor (GCR, human NR3C1 gene) transcription factor, resulting in transcriptional activation and repression of various GCR-responsive genes. We tested for differential gene expression with a multiplexed panel of 250 gene expression panel using the Nanostring nCounter(R) system. Gene panel selection was based on membership of genes in canonical KEGG pathways for tight-junction, adherens junction, focal adhesion, actin cytoskeleton regulation, and colorectal cancer. Our TEER results confirm, as previously reported, that long-term Dexamethasone exposure results in decreased permeability in Caco-2 monolayers ~day 20-25. Culture age and Dexamethasone exposure both contributed to differential gene expression for cell-cell junction, protein kinases, survival and cancer associated genes, reported here in the context of their corresponding KEGG pathway representations. The findings give evidence for GC and time-associated patterns of transcriptional response and provide further insight into long-term glucocorticoid-associated physiological effects on the gastrointestinal epithelia. Future research utilizing more advanced cell culture methods will use this data-set as a reference.

cell biology↗

bioRxiv2018

Using LASSO in gene co-expression network for genome-wide identification of gene interactions responding to salt stress in rice

In many applications, such as gene co-expression network analyses, data arises with a huge number of covariates while the size of sample is comparatively small. To improve the accuracy of prediction, variable selection is often used to get a sparse solution by forcing coefficients of variables contributing less to the observed response variable to zero. Various algorithms were developed for variable selection, but LASSO is well known for its statistical accuracy, computational feasibility and broad applicability to adaptation. In this project, we applied LASSO to the gene co-expression network of rice with salt stress to discover key gene interactions for salt-tolerance related phenotypes. The dataset we have is a high-dimensional one, having 50K genes from 100 samples, with the issue of multicollinearity for fitting linear regression - the expression level of genes in the same pathway tends to be highly correlated. The property of LASSO with sparse parameters is naturally suitable to identify gene interactions of interest in this dataset. After biologically functional modules in the co-expression network was identified, the major changed expression patterns were further selected by LASSO regression to establish a linear relationship between gene expression profiles and physiological responses, such as sodium/potassium condenses, with salt stress. Five modules of intensively co-expressed genes, from 45 to 291 genes, were identified by our method with significant P-values, which indicate these modules are significantly associated with physiological responses to stress. Genes in these modules have functions related to ion transport, osmotic adjustment, and oxidative tolerance. For example, LOC_Os7g47350 and LOC_Os07g37320 are co-expressed gene in the same module 15. Both are ion transporter genes and have higher gene expression levels for rice with low sodium levels with salt stress.

bioinformatics↗

bioRxiv2018

Whole genome scan reveals the multigenic basis of recent tidal marsh adaptation in a sparrow

Natural selection acts on functional molecular variation to create local adaptation, the \"good fit\" we observe between an organisms phenotype and its environment. Genomic comparisons of lineages in the earliest stages of adaptive divergence have high power to reveal genes under natural selection because molecular signatures of selection on functional loci are maximally detectable when overall genomic divergence is low. We conducted a scan for local adaptation genes in the North American swamp sparrow (Melospiza georgiana), a species that includes geographically connected populations that are differentially adapted to freshwater vs. brackish tidal marshes. The brackish tidal marsh form has rapidly evolved tolerance for salinity, a deeper bill, and darker plumage since colonizing coastal habitats within the last 15,000 years. Despite their phenotypic differences, background genomic divergence between these populations is very low, rendering signatures of natural selection associated with this recent coastal adaptation highly detectable. We recovered a multigenic snapshot of ecological selection via a whole genome scan that revealed robust signatures of selection at 31 genes with functional connections to bill shape, plumage melanism and salt tolerance. As in Darwins finches, BMP signaling appears responsible for changes in bill depth, a putative magic trait for ecological speciation. A signal of selection at BNC2, a melanocyte transcription factor responsible for human skin color saturation, implicates a shared genetic mechanism for sparrow plumage color and human skin tone. Genes for salinity tolerance constituted the majority of adaptive candidates identified in this genome scan (23/31) and included vasoconstriction hormones that can flexibly modify osmotic balance in tune with the tidal cycle by influencing both drinking behavior and kidney physiology. Other salt tolerance genes had potential pleiotropic effects on bill depth and melanism (6/31), offering a mechanistic explanation for why these traits have evolved together in coastal swamp sparrows, and in other organisms that have converged on the same \"salt marsh syndrome\". As a set, these candidates capture the suite of physiological changes that coastal swamp sparrows have evolved in response to selection pressures exerted by a novel and challenging habitat.

evolutionary biology↗

bioRxiv2018

Systematic assessment of GFP tag position on protein localization and growth fitness in yeast

While protein tags are ubiquitously utilized in molecular biology, they harbor the potential to interfere with functional traits of their fusion counterparts. Systematic evaluation of the effect of protein tags on localization and function would promote accurate use of tags in experimental setups. Here we examine the effect of Green Fluorescent Protein (GFP) tagging at either the N or C terminus of budding yeast proteins on localization and functionality. We use a competition-based approach to decipher the relative fitness of two strains tagged on the same protein but on opposite termini and from that infer the correct, physiological localization for each protein and the optimal position for tagging. Our study provides a first of a kind systematic assessment of the effect of tags on the functionality of proteins and provides step towards broad investigation of protein fusion libraries.\n\nHighlightsO_LIProtein tags are widely used in molecular biology although they may interfere with protein function.\nC_LIO_LIThe subcellular localization of hundreds of proteins in yeast is different when tagged at the N or the C terminus.\nC_LIO_LIA competition based assay enables systematic deciphering of correct tagging terminus for essential proteins.\nC_LIO_LIThe presented approach can be used to derive physiologically relevant tagged libraries.\nC_LI

cell biology↗

bioRxiv2018

Macrophage-Dependent Trafficking and Remodeling of the Basement Membrane-Interstitial Matrix Interface

Macrophages infiltrate and remodel extracellular matrix barriers during development and disease. Bahr and Weiss demonstrate that human macrophages remodel native basement membrane barriers in an MT1-MMP-dependent fashion while retaining the ability to traverse tissue barriers by actomyosin-dependent forces alone.\n\nAbstractMacrophages dominate inflammatory environments where they modify the extracellular matrix by mobilizing complex repertoires of proteolytic enzymes. Nevertheless, the dominant proteinases used by macrophage as they confront physiologic tissue barriers remain undefined. Herein, we have characterized the molecular mechanisms that define human macrophage-extracellular matrix interactions ex vivo. Resting and immune-polarized macrophages are shown to proteolytically remodel basement membranes while infiltrating the underlying interstitial matrix. In an unbiased screen to identify key proteases, we find that the macrophage metalloproteinase, MT1-MMP, is the dominant effector of basement membrane degradation and invasion. Unexpectedly, macrophages can alternatively use actomyosin-dependent forces to transmigrate native basement membrane pores that provide cells with proteinase-independent access to the interstitial matrix. These studies not only identify MT1-MMP as a key proteolytic effector of extracellular matrix remodeling by human macrophages, but also define the invasive strategies used by macrophages to traverse physiologic tissue barriers.

immunology↗

bioRxiv2018

Dominance rank-associated immune gene expression is widespread, sex-specific, and a precursor to high social status in wild male baboons

In humans and other hierarchical species, social status is tightly linked to variation in health and fitness-related traits. Experimental manipulations of social status in female rhesus macaques suggest that this relationship is partially explained by status effects on immune gene regulation. However, social hierarchies are established and maintained in different ways across species: while some are based on kin-directed nepotism, others emerge from direct physical competition. We investigated how this variation influences the relationship between social status and immune gene regulation in wild baboons, where hierarchies in males are based on fighting ability but female hierarchies are nepotistic. We measured rank-related variation in gene expression levels in adult baboons of both sexes at baseline and in response to ex vivo stimulation with the bacterial endotoxin lipopolysaccharide (LPS). We identified >2000 rank- associated genes in males, an order of magnitude more than in females. In males, high status predicted increased expression of genes involved in innate immunity and preferential activation of the NFkB-mediated pro-inflammatory pathway, a pattern previously associated with low status in female rhesus macaques. Using Mendelian randomization, we reconcile these observations by demonstrating that high status-associated gene expression patterns are precursors, not consequences, of high social status in males, in support of the idea that physiological condition determines who attains high rank. Together, our work provides the first test of the relationship between social status and immune gene regulation in wild primates. It also emphasizes the importance of social context in shaping the relationship between social status and immune function.\n\nSIGNIFICANCESocial status predicts fitness outcomes in social animals, motivating efforts to understand its physiological causes and consequences. We investigated the relationship between social status and immune gene expression in wild baboons, where female status is determined by kinship but male status is determined by fighting ability. We uncover pervasive status-gene expression associations in males, but not females. High status males exhibit high levels of pro-inflammatory gene expression, in contrast to previous findings in hierarchies that are not competitively determined. Using Mendelian randomization, we show that this status-associated variation precedes dominance rank attainment: males who compete successfully for high status are already immunologically distinct. The nature of social hierarchies thus fundamentally shapes the relationship between social status and immune function.

evolutionary biology↗

bioRxiv2018

miR-263b controls circadian rhythms and structural plasticity of small ventral lateral neurons by inhibition of Beadex

Circadian clocks drive rhythmic physiology and behavior to allow adaption to daily environmental changes. In Drosophila, the small ventral lateral neurons (sLNvs) are the master pacemakers that control circadian rhythms. Circadian changes are observed in the dorsal axonal projections of the sLNvs, but their physiological importance and the underlying mechanism are unclear. Here we identified miR-263b as an important regulator of circadian rhythms in Drosophila. Flies depleted of miR-263b (miR-263bKO) exhibited dramatically impaired rhythms under constant darkness. Indeed, miR-263b is rhythmically expressed and controls circadian output by affecting the structural plasticity of sLNvs through inhibition of expression of the LIM-only protein Beadex (Bx). The misexpression of Bx in flies phenocopied miR-263bKO in behavior and molecular characteristics. In addition, the circadian phenotypes of miR-263bKO were recapitulated by mutating the miR-263b binding sites in the Bx 3'UTR. Together, these results establish miR-263b as an important regulator of circadian locomotor behavior.

neuroscience↗

bioRxiv2018

The Female Heart: Sex Differences in the Signal Dynamics of ECG in Response to Stress

Sex differences in the study of the human physiological response to mental stress are often erroneously ignored. To this end, we set out to show that our understanding of the stress response is fundamentally altered once sex differences are taken into account. This is achieved by comparing the heart rate variability (HRV) signals acquired during mental maths tests from ten females and ten males of similar maths ability; all females were in the follicular phase of their menstrual cycle. For rigour, the HRV signals from this pilot study were analysed using temporal, spectral and nonlinear signal processing techniques, which all revealed significant statistical differences between the sexes, with the stress-induced increases in the heart rates from the males being significantly larger than those from the females (p-value=2.2x10-3). In addition, mental stress produced an overall increase in the power of the low frequency component of HRV in the males, but caused an overall decrease in the females. The stress-induced changes in the power of the high frequency component were even more profound; it greatly decreased in the males, but increased in the females. We also show that mental stress was followed by the expected decrease in sample entropy, a nonlinear measure of signal regularity, computed from the males HRV signals, while overall, stress manifested in an increase in the sample entropy computed from the females HRV signals. This finding is significant, since mental stress is commonly understood to be manifested in the decreased entropy of HRV signals, however, the significant difference (p-value=2x10-9) in the changes in the entropies from the males and females highlights the pitfalls in ignoring sex in the formation of a physiological hypothesis. Furthermore, it has been argued that oestrogen attenuates the effect of catecholamine stress hormones; the findings from this investigation suggest for the first time that the conventionally cited cardiac changes, attributed to the fight-or-flight stress response, are not universally applicable to females. Instead, this pilot study provides an alternative interpretation of cardiac responses to stress in females, which indicates a closer alignment to the evolutionary tend-and-befriend response.

bioengineering↗

bioRxiv2018

Modeling Cellular Resource Allocation Reveals Low Phenotypic Plasticity of C4 Plants and Infers Environments of C4 Photosynthesis Evolution

- The regulation of resource allocation in biological systems observed today is the cumulative result of natural selection in ancestral and recent environments. To what extent are observed resource allocation patterns in different photosynthetic types optimally adapted to current conditions, and to what extend do they reflect ancestral environments? Here, we explore these questions for C3, C4, and C3-C4 intermediate plants of the model genus Flaveria.\n- We developed a detailed mathematical model of carbon fixation, which accounts for various environmental parameters and for energy and nitrogen partitioning across photosynthetic components. This allows us to assess environment-dependent plant physiology and performance as a function of resource allocation patterns.\n- To achieve maximal CO2 fixation rates under growth conditions differing from those experienced during their evolution, C4 species need to re-allocate significantly more nitrogen between photosynthetic components than their C3 relatives. As this is linked to a limited phenotypic plasticity, observed resource distributions in C4 plants still reflect optimality in ancestral environments, allowing their quantitative inference.\n- Our work allows us to quantify environmental effects on resource allocation and performance of photosynthetic organisms. This understanding paves the way for interpreting present photosynthetic physiology in the light of evolutionary history.

plant biology↗

bioRxiv2018

Sex makes them sleepy: change in host reproductive status induces diapause in parasitoids

When organisms coevolve, any change in one species can induce phenotypic changes in traits and ecology of the other species. The role such interactions play in ecosystems is central, but their mechanistic bases remain underexplored. Upper trophic level species have to synchronize their life-cycle to both abiotic conditions and to lower trophic level species phenology and phenotypic variations. We tested the effect of host seasonal strategy on parasitoid diapause induction by using a holocyclic clone of the pea aphid Acyrthosiphon pisum producing asexual and sexual morphs that are viviparous females (i.e. laying embryos) and oviparous females (laying eggs), respectively, the latter being only present at the end of the growing season. Aphidius ervi parasitoids from populations of contrasted climatic origin (harsh vs. mild winter areas) were allowed to parasitize each morph in a split-brood design and developing parasitoids were next reared under either fall-like or summer-like temperature-photoperiod conditions. We next examined aspects of the host physiological state by comparing the relative proportion of forty-seven metabolites and lipid reserves in both morphs produced under the same conditions. We found that oviparous morphs are cues per se for diapause induction; parasitoids entered diapause at higher levels when developing in oviparous hosts (19.4 {+/-} 3.0%) than in viviparous ones (3.6 {+/-} 1.3%), under summer-like conditions (i.e., when oviparous aphids appear in the fields). This pattern was only observed in parasitoids from the harsh winter area since low diapause levels were observed in the other population, suggesting local adaptations to overwintering cues. Metabolomics analyses show parasitoids response to be mainly influenced by the hosts physiology, with higher proportion of polyols and sugars, and more fat reserves being found in oviparous morphs. Host quality thus varies across the seasons and represents one of the multiple environmental parameters affecting parasitoid diapause. Our results underline strong coevolutionary processes between hosts and parasitoids in their area of origin, likely leading to phenological synchronization, and we point out the importance of such bottom-up effects for trait expression, and for the provision of ecosystem services such as biological control in the context of climate change.

ecology↗