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High-resolution vasomotion analysis reveals novel venous physiological features and progressive modulation of cerebral vascular networks by stroke

Spontaneous cerebral vasomotion, characterized by [~]0.1 Hz rhythmic contractility, is crucial for brain homeostasis. However, our understanding of vasomotion is limited due to a lack of high-precision analytical methods to determine single vasomotion events at basal levels. Here, we developed a novel strategy that integrates a baseline smoothing algorithm, allowing precise measurements of vasodynamics and concomitant Ca2+ dynamics in mouse cerebrovasculature imaged by two-photon microscopy. We identified several previously unrecognized vasomotion properties under different physiological and pathological conditions, especially in ischemic stroke, which is a highly harmful brain disease that results from vessel occlusion. First, the dynamic characteristics between SMCs Ca2+ and corresponding arteriolar vasomotion are interplayed. Second, compared to previous diameter-based estimations, our radius-based measurements reveal nonisotropic vascular movements, enabling a more precise determination of the latency between smooth muscle cell (SMC) Ca2+ activity and vasocontraction. Third, we characterized single vasomotion event kinetics at scales of less than 4 seconds. Finally, following pathological vasoconstrictions induced by ischemic stroke, vasoactive arterioles transitioned to an inert state and persisted despite recanalization. In summary, we developed a highly accurate technique for analyzing spontaneous vasomotion, and we suggest a potential strategy to reduce stroke damage by promoting vasomotion recovery.

neuroscience↗

The sleep quality- and myopia-linked PDE11A-Y727C variant impacts neural physiology by reducing catalytic activity and altering subcellular compartmentalization of the enzyme

Recently, a Y727C variant in the dual-specific 3,5-cyclic nucleotide phosphodiesterase 11A (PDE11A-Y727C) was linked to increased sleep quality and reduced myopia risk in humans. Given the well-established role that the PDE11 substrates cAMP and cGMP play in eye physiology and sleep, we determined if 1) PDE11A protein is expressed in the retina or other eye segments in mouse, 2) PDE11A-Y7272C affects catalytic activity and/or subcellular compartmentalization more so than the nearby suicide-associated PDE11A-M878V variant, and 3) Pde11a deletion alters eye growth or sleep quality in male and female mice. Western blots show distinct protein expression of PDE11A4, but not PDE11A1-3, in eyes of Pde11a WT--but not KO mice--that vary by eye segment and age. In HT22 and COS-1 cells, PDE11A4-Y727C reduces PDE11A4 catalytic activity far more than PDE11A4-M878V, with both variants reducing PDE11A4-cAMP more so than PDE11A4-cGMP activity. Despite this, Pde11a deletion does not alter age-related changes in retinal or lens thickness, axial length, nor vitreous or anterior chamber depth. Further, Pde11a deletion only minimally changes refractive error and sleep quality. That said, both variants also dramatically alter the subcellular compartmentalization of human and mouse PDE11A4, an effect occurring independently of dephosphorylating PDE11A4-S117/S124 or phosphorylating PDE11A4-S162. Rather, re-compartmentalization of PDE11A4-Y727C is due to the loss of the tyrosine changing how PDE11A4 is packaged/repackaged via the trans-Golgi network. Therefore, the protective impact of the Y727C variant may reflect a gain-of-function (e.g., PDE11A4 displacing another PDE) that warrants further investigation in the context of reversing/preventing sleep disturbances or myopia.

neuroscience↗

Mapping the physiological changes in sleep regulation across infancy and young childhood

Sleep patterns in infancy and early childhood vary greatly and change rapidly during development. In adults, sleep patterns are regulated by interactions between neuronal populations in the brainstem and hypothalamus, driven by the circadian and sleep homeostatic processes. However, the neurophysiological mechanisms underlying the sleep patterns and their variations across infancy and early childhood are poorly understood. We investigated whether a well-established mathematical model for sleep regulation in adults can model infant sleep characteristics and explain the physiological basis for developmental changes. By fitting longitudinal sleep data spanning 2 to 540 days after birth, we inferred parameter trajectories across age. We found that the developmental changes in sleep patterns are consistent with a faster accumulation and faster clearance of sleep homeostatic pressure in infancy and a weaker circadian rhythm in early infancy. We also find greater sensitivity to phase-delaying effects of light in infancy and early childhood. These findings reveal fundamental mechanisms that regulate sleep in infancy and early childhood. Given the critical role of sleep in healthy neurodevelopment, this framework could be used to pinpoint pathophysiological mechanisms and identify ways to improve sleep quality in early life.

neuroscience↗

Parvalbumin interneuron mGlu5 receptors govern sex differences in prefrontal cortex physiology and binge drinking

Despite established sex differences in the prevalence and presentation of psychiatric disorders, little is known about the cellular and synaptic mechanisms that guide these differences under basal conditions. Proper function of the prefrontal cortex (PFC) is essential for the top-down regulation of motivated behaviors. Activity of the PFC is tightly controlled by parvalbumin-expressing interneurons (PV-INs), a key subpopulation of fast-spiking GABAergic cells that regulate cortical excitability through direct innervations onto the perisomatic regions of nearby pyramidal cells. Recent rodent studies have identified notable sex differences in PV-IN activity and adaptations to experiences such as binge drinking. Here, we investigated the cellular and molecular mechanisms that underlie sex-specific regulation of PFC PV-IN function. Using whole-cell patch clamp electrophysiology and selective pharmacology, we report that PV-INs from female mice are more excitable than those from males. Moreover, we find that mGlu1 and mGlu5 metabotropic glutamate receptors regulate cell excitability, excitatory drive, and endocannabinoid signaling at PFC PV-INs in a sex-dependent manner. Genetic deletion of mGlu5 receptors from PV-expressing cells abrogates all sex differences observed in PV-IN membrane and synaptic physiology. Lastly, we report that female, but not male, PV-mGlu5-/- mice exhibit decreased voluntary drinking on an intermittent access schedule, which could be related to changes in ethanols stimulant properties. Importantly, these studies identify mGlu1 and mGlu5 receptors as candidate signaling molecules involved in sex differences in PV-IN activity and behaviors relevant for alcohol use.

neuroscience↗

CO2 Reduction by the Iron Nitrogenase Competes with N2 Fixation Under Physiological Conditions

Nitrogenases are the only known enzymes that reduce molecular nitrogen (N2) to ammonia. Recent findings have demonstrated that nitrogenases also reduce the greenhouse gas carbon dioxide (CO2), suggesting CO2 to be a competitor of N2. Intriguingly, nitrogenase isoforms (i.e., molybdenum (Mo), vanadium and iron (Fe) nitrogenase) differ significantly in their ability to reduce CO2, but the mechanisms underlying these differences remain elusive. Here, we study the competing reduction of CO2 and N2 by the two nitrogenases of Rhodobacter capsulatus, the Mo and Fe nitrogenase. Analyzing their full CO2 reduction product spectrum in vitro, we find the Fe nitrogenase almost three-fold more efficient in CO2 reduction than the Mo isoform. Furthermore, the in vitro competition experiments reveal the Fe nitrogenase to be profoundly less selective for the reduction of N2 than the Mo nitrogenase. We observe the same effects in vivo, where adding CO2 drastically increases the doubling times of diazotrophically grown R. capsulatus strains that rely on the Fe nitrogenase. The Fe nitrogenase-dependent R. capsulatus strains reduce CO2 to methane under physiological conditions, highlighting the potential of the Fe nitrogenase for the biotechnological conversion of CO2 into value-added compounds. Furthermore, both products are secreted into the surrounding, potentially influencing the composition of microbial communities in Mo-deficient environments.

biochemistry↗

A potential pathway that links intron retention with the physiological recovery by a Japanese herbal medicine

Our previous experiments with klotho mice (i.e., klotho knockout mice) showed that aberrant intron retention (IR) occurs in a pre-symptomatic state of aging and can be restored to the normal state by administration of Juzentaihoto (JTT), a formula of the Japanese herbal medicine (referred to as kampo; Okada et al., 2021). To explain that this phenomenon is not just a specific example observed in klotho mice, but is due to a universal cause that may be common in a pre-symptomatic state, we re-analyzed the data for genes that were differentially expressed in the klotho liver in response to JTT. Our data showed that AMPK signaling was activated in these mice, resulting in inhibition of anabolic pathways including protein synthesis and activation of catabolic pathways including lipolysis in various organs. These data were consistent with the observation that klotho mice appeared to be in a perpetual state of pseudo-starvation, i.e., based on their overall metabolic profile. The abnormally increased incidence of IR (IncIR) in the liver of klotho mice could be classified into three types according to their transcriptional status, revealing that each of all the three types of IncIR was caused by AMPK activation, a consequence of the pseudo-starvation state exhibited by these mice. Furthermore, we showed that both the transcriptional drift variance and the IR drift variance can be useful for visually assessing recovery from the pseudo-starvation state of klotho mice after administration of JTT. With these data, we propose a novel pathway linking intron retention to changes in the physiological state such as starvation, resulting in the maintenance of cellular homeostasis.

bioinformatics↗

Escape problem of magnetotactic bacteria - physiological magnetic field strength help magnetotactic bacteria navigate in simulated sediments

Bacterial motility is typically studied in bulk solution, while their natural habitats often are complex environments. Here, we produced microfluidic channels that contained sediment-mimicking obstacles to study swimming of magnetotactic bacteria in a near-realistic environment. Magnetotactic bacteria are microor-ganisms that form chains of nanomagnets and that orient in Earths magnetic field. The obstacles were produced based on micro-computer tomography reconstructions of bacteria-rich sediment samples. We characterized the swimming of the cells through these channels and found that swimming throughput was highest for physiological magnetic fields. This observation was confirmed by extensive computer simulations using an active Brownian particle model, which were parameterized based on experimental trajectories, in particular with the trajectories near the sediment-mimicking obstacles, from which the interactions of the swimming bacteria with the obstacles were determined. The simulations were used to quantify the swimming throughput in detail. They showed the behavior seen in experiments, but also exhibited considerable variability between different channel geometries. The simulations indicate that swimming at strong fields is impeded by the trapping of bacteria in "corners" that require transient swimming against the magnetic field for escape. At weak fields, the direction of swimming is almost random, making the process inefficient as well. We confirmed the trapping effect in our experiments and showed that lowering the field strength allows the bacteria to escape. We hypothesize that over the course of evolution, magnetotactic bacteria have thus evolved to produce magnetic properties that are adapted to the geomagnetic field in order to balance movement and orientation in such crowded environments.

biophysics↗

Inhibition of hERG K channels by verapamil at physiological temperature: Implications for the CiPA Initiative

The Comprehensive in vitro Proarrhythmia Assay (CiPA) initiative reassesses using the inhibition of hERG channels by drugs as the major determinant for assessment of a drugs potential to cause Torsades de Pointes (TdP) cardiac arrhythmias. Here we report on one phase of CiPA: independent determination of hERG inhibitory properties in order to test the reproducibility of data gathered in different labs and the practicality of using the CiPA-defined recording conditions. We measured inhibition of hERG1a potassium channels stably expressed in HEK293 cells using manual whole-cell patch-clamp electrophysiology recordings at the physiological temperature of 37{degrees}C by verapamil, a known hERG inhibitor. We report that the IC50 for inhibition (180.4nM) and the Hill coefficient (1.4) for verapamil measured in an academic lab were similar to the IC50 (204nM) and Hill coefficient (0.9) measured at the Food and Drug Administration labs, indicating low variability in measurements between labs. We report that the CiPA step voltage protocol, a series of voltage steps characterized by 10 second duration depolarizing pulses at 37{degrees}C, resulted in a very low (5%) experimental success rate per cell in our hands. To circumvent the low success rate, we shortened the duration of the depolarizing pulse to 3 seconds (from 10 seconds) and shortened the duration of interpulse intervals, which is more consistent with the duration of voltage pulses used in biophysical studies of hERG, such that the entire revised protocol was shortened from over 30 minutes to approximately 10 minutes in duration. Using the revised protocol, we found an IC50 of inhibition by verapamil of 210.5 nM and Hill coefficient of 1.2. These values were similar to those generated using the original, longer CiPA step protocol. Furthermore, our success rate using the shortened protocol rose to 25%, an increase of 5-fold over the initial protocol. In summary, we captured key pharmacological data for subsequent analysis in CiPA using a revised, shorter protocol with an enhanced success rate and an overall enhanced feasibility. We propose the shorter protocol is more pragmatic for generation of hERG channel drug inhibition data for CiPA and other regulatory sciences.

pharmacology and toxicology↗

Physiological and transcriptomic response to methyl-coenzyme M reductase limitation in Methanosarcina acetivorans

Methyl-coenzyme M reductase (MCR) catalyzes the final step of methanogenesis, the microbial metabolism responsible for nearly all biological methane emissions to the atmosphere. Decades of biochemical and structural studies have generated detailed insights into MCR function in vitro, yet very little is known about the interplay between MCR and methanogen physiology. For instance, while it is routinely stated that MCR catalyzes the rate-limiting step of methanogenesis, this statement has not been categorically tested. Here, to gain a more direct understanding of MCRs control on the growth of Methanosarcina acetivorans, we generate a strain with an inducible mcr operon on the chromosome, allowing for careful control of MCR expression. We show that MCR is not growth rate limiting in substrate-replete batch cultures. However, through careful titration of MCR expression, growth-limiting state(s) can be obtained. Transcriptomic analysis of M. acetivorans experiencing MCR-limitation reveals a global response with hundreds of differentially expressed genes across diverse functional categories. Notably, MCR limitation leads to a strong induction of methylsulfide methyltransferases, likely due to insufficient recycling of metabolic intermediates. In addition, the mcr operon does not seem to be transcriptionally regulated, i.e., it is constitutively expressed, suggesting that the overabundance of MCR might be beneficial when cells experience nutrient limitation or stressful conditions. Altogether, we show that there is wide range of cellular MCR concentrations that can sustain optimal growth, suggesting that other factors like anabolic reactions might be rate-limiting for methanogenic growth. ImportanceMethane is a potent greenhouse gas that has contributed to ca. 25% of global warming in the post-industrial era. Atmospheric methane is primarily of biogenic origin, mostly produced by microorganisms called methanogens. In methanogens, methyl-coenzyme M reductase (MCR) catalyzes methane formation. Even though MCR comprises ca. 10% of the cellular proteome, it is hypothesized to be growth-limiting during methanogenesis. Here, we show that Methanosarcina acetivorans grown under standard laboratory conditions produces more MCR than its cellular demand for optimal growth. The tools outlined in this study can be used to refine metabolic models of methanogenesis and assay lesions in MCR in a higher throughput manner than isolation and biochemical characterization of pure protein.

microbiology↗

Metabolic responses to cold: thermal physiology of native common waxbills (Estrilda astrild)

Ecophysiological studies of invasive species tend to focus on captive individuals and their invasive range. However, the importance of gaining a thorough understanding of their physiology in their native range, where autecological knowledge is limited, has played a crucial role in assessing species ecophysiological responses to the often novel environmental conditions encountered in their invasive range. Here, we investigated the ecophysiological characteristics of a population of the wild-caught common waxbill (Estrilda astrild), a successful global invader, in part of its native range (South Africa). We investigated how this species adjusts its resting metabolic rate over a range of temperatures to identify its thermoneutral zone (TNZ) as an indicator of a species thermal tolerance. The observed TNZ curve predominantly followed the classic Scholander-Irving model, with metabolic rates increasing linearly at temperatures outside the TNZ. However, we found an inflection point at moderately cold temperatures (16{degrees}C) where the common waxbill began to decrease its metabolic rate. This finding highlights the potential use of an energy-saving strategy as an adaptive response to cold, such as facultative hypothermic responses through a reduction in body temperature, which may explain their success as an invasive species. We argue that although metabolic infection points have been repeatedly identified in studies of TNZ, the specific mechanisms behind metabolic down-regulation at low temperatures remain underexplored in the literature. We therefore suggest that future research should focus on investigating body temperature variation, with particular emphasis on its potential contribution to metabolic adaptation in colder environments.

ecology↗

Depot-Specific mRNA Expression Programs in Human Adipocytes Suggest Physiological Specialization via Distinct Developmental Programs

Adipose tissue is distributed in diverse locations throughout the human body. Not much is known about the extent to which anatomically distinct adipose depots are functionally distinct, specialized organs, nor whether depot-specific characteristics result from intrinsic developmental programs, as opposed to reversible physiological responses to differences in tissue microenvironment. We used DNA microarrays to compare mRNA expression patterns of isolated human adipocytes and cultured adipose stem cells, before and after ex vivo adipocyte differentiation, from seven anatomically diverse adipose tissue depots. Adipocytes from different depots displayed distinct gene-expression programs, which were most closely shared with anatomically related depots. These depot-specific differences in gene expression were recapitulated when adipocyte progenitor cells from each site were differentiated ex vivo, suggesting that progenitor cells from specific anatomic sites are deterministically programmed to differentiate into depot-specific adipocytes. mRNAs whose expression differed between anatomically diverse groups of depots (e.g., subcutaneous vs. internal) suggest important functional specializations. Many developmental transcription factors showed striking depot-specific patterns of expression, suggesting that adipocytes in each anatomic depot are programmed during early development in concert with anatomically related tissues and organs. Our results support the hypothesis that adipocytes from different depots are functionally distinct and that their depot-specific specialization reflects distinct developmental programs.

developmental biology↗

SbPIP2 Mediated Improvements in Plant Resilience: Physiological and Molecular Insights into Abiotic Stress Response

Understanding the mechanisms behind plant resilience to abiotic stresses is essential for enhancing crop yield and sustainability. This study integrates findings from a comprehensive investigation into the function of the SbPIP2 gene, which encodes an aquaporin protein, in improving the abiotic stress tolerance of transgenic plants. Our integrated approach revealed that transgenic plants overexpressing SbPIP2 significantly reduce reactive oxygen species (ROS) accumulation and exhibit enhanced physiological attributes, including higher seed germination rates, improved growth, early flowering, and better seed setting under stress conditions. Notably, these plants also showed a quicker recovery and completion of their lifecycle post-stress treatment. The transcriptomic analysis provided a deeper understanding of the genetic modifications contributing to stress resilience, highlighting the involvement of genes associated with oxidative stress response, calcium and sugar signaling pathways, stomatal regulation, phytohormone biosynthesis, and flower development. Additionally, the study underscores the central role of abscisic acid (ABA) in mediating stress responses through hormonal regulation, with transgenic plants displaying increased ABA levels due to the upregulation of biosynthesis genes and downregulation of catabolism genes. This hormonal adjustment is critical for stomatal closure, reducing water loss, and enhancing tolerance to abiotic stresses. Our findings elucidate the complex genetic and molecular pathways that underpin abiotic stress tolerance in plants, offering valuable insights for future research aimed at improving crop resilience through genetic engineering, thereby addressing the challenges of climate change and environmental stressors.

plant biology↗

Evaluating computational efforts and physiological resolution of mathematical models of cardiac tissue

Computational techniques have significantly advanced our understanding of cardiac electrophysiology, yet they have predominantly concentrated on averaged models that do not represent the intricate dynamics near individual cardiomyocytes. Recently, accurate models representing individual cells have gained popularity, enabling analysis of the electrophysiology at the micrometer level. Here, we evaluate five mathematical models to determine their computational efficiency and physiological fidelity. Our findings reveal that cell-based models introduced in recent literature offer both efficiency and precision for simulating small tissue samples (comprising thousands of cardiomy-ocytes). Conversely, the traditional bidomain model and its simplified counterpart, the monodomain model, are more appropriate for larger tissue masses (encompassing millions to billions of cardiomyocytes). For simulations requiring detailed parameter variations along individual cell membranes, the EMI model emerges as the only viable choice. This model distinctively accounts for the extracellular (E), membrane (M), and intracellular (I) spaces, providing a comprehensive framework for detailed studies. Nonetheless, the EMI models applicability to large-scale tissues is limited by its substantial computational demands for subcellular resolution.

biophysics↗

Assessing the Effects of Various Physiological Signal Modalities on Predicting Different Human Cognitive States

Robust estimation of systemic human cognitive states is critical for many applications, from simply detecting inefficiencies in human task performance to adapting the behaviors of artificial agents to improve team performance in mixed-initiative human-machine teams. Here we use comprehensive analyses of a multi-modal dataset from a multi-tasking driving experiment to provide systematic evidence that percentage change in pupil size (PCPS) in human eye gaze is the most reliable biomarker for assessing three human cognitive states relevant to task performance: workload, sense of urgency, and mind wandering. Specifically, we performed comprehensive statistical tests that establish the superior performance of PCPS compared other physiological signals like electroencephalogram (EEG), functional near-infrared spectroscopy (fNIRS), respiration, arterial blood pressure (ABP), and skin conductance. Based on the eye gaze data, we also characterized the relation between workload and sense of urgency, observing that consecutive occurrences of higher sense of urgency tended to increase overall workload. We also trained five state-of-the-art machine learning models on the data to determine their potential for predicting the three systemic cognitive states across subjects, showing that four of them had similar highest accuracy in cognitive state classification based on PCPS (with one, random forest, showing inferior performance). In combination with the statistical analyses, the comparative modeling results demonstrate that PCPS, in contrast to prior findings in the literature, represents the optimal method for estimating the three performance-relevant cognitive states.

neuroscience↗

Persistent Behavioral and Physiological Effects of Dietary Protein Restriction

Protein provides essential amino acids critical for survival. Recent research has identified that dietary protein restriction induces physiological and behavioral adaptations and that those adaptations are mediated by liver-produced fibroblast growth factor 21 (FGF21) that acts in the brain. Most of the research on adaptations to dietary protein restriction and the biological factors that mediate those adaptations carries an implicit assumption that the effects of dietary protein restriction are reversible. Rarely is the assumption of reversibility directly examined by varying dietary protein content within animals. Recently collected data on preference for protein versus carbohydrate solutions indicates that when mice are placed on a low (5%) protein diet, preference for protein is rapidly increased. However, when mice are switched from a low to normal (20%) protein diet, relative consumption of protein decreases but preference for protein persists. Re-analysis of published data suggests, similarly, that preference for protein-rich food sources remains elevated following exposure to dietary protein restriction and that calcium influx in the ventral tegmental area of the brain in response to protein consumption also remains persistently elevated following dietary protein restriction. Together, the data suggest that prior protein restriction can exert long-lasting effects on protein preference and on brain activity associated with protein consumption. The finding that the effects of protein restriction do not rapidly reverse implies that protein choice may be a function, not only of current nutritional state, but of historical nutritional conditions. Further, these results suggest that a full understanding of the environmental and biological determinants of protein choice requires studies in which dietary protein intake is varied within subjects.

animal behavior and cognition↗

Structural insights into physiological activation and antagonism of melanin-concentrating hormone receptor MCHR1

Melanin-concentrating hormone (MCH) is a 19-amino-acid neuropeptide playing crucial roles in energy homeostasis, sleep, and various physiological processes. It acts through two G protein-coupled receptors, MCHR1 and MCHR2, with MCHR1 being universally present in mammals and a potential target for treating metabolic and mental health conditions. However, drug development efforts have been impeded by the lack of structural information. Here, we present the cryo-EM structures of MCHR1 in its active state complexed with MCH and Gi1, as well as in its inactive state bound to a selective antagonist SNAP-94847. Structural and mutagenesis analyses disclosed the recognition mechanisms for both MCH and SNAP-94847, the activation mechanism and antagonism of MCHR1, and the determinants of ligand specificity. These findings are expected to accelerate the development of better drugs targeting the MCH system.

biophysics↗

Pseudogenisation of NK3 Homeobox 2 (Nkx3.2) in Monotremes Provides Insight into Unique Gastric Anatomy and Physiology

Development of the vertebrate antral stomach and pyloric sphincter (antropyloric region) - involved in enzymatic breakdown and thoroughfare of food - is underpinned by a highly conserved developmental pathway involving the hedgehog, bone morphogenetic protein (BMP) and Wingless/Int-1 (Wnt) protein families. Monotremes are a unique lineage where acid-based digestion has been lost, and this correlates with a lack of genes for gastric acid and enzymes in the genomes of the platypus (Ornithorhynchus anatinus) and short-beaked echidna (Tachyglossus aculeatus). Furthermore, these species feature unique gastric phenotypes, both with truncated and aglandular antral stomachs and the platypus with no pylorus. Here, we explore the genetic underpinning of monotreme gastric phenotypes, investigating genes important in antropyloric development using the newest monotreme genome sequences (mOrnAna1.pri.v4 and mTacAcu1) together with RNA-seq data. We found that the pathway is generally conserved but, NK3 homeobox 2 (Nkx3.2) was pseudogenised in both platypus and echidna. We speculate that pyloric-like restriction in the echidna may correlate with independent evolution of Grem1 and Bmp4 sequences, and that the convergent loss of gastric acid and stomach size genotypes and phenotypes in teleost and monotreme lineages may be a result of eco-evolutionary dynamics. These findings reflect the effects of gene loss on phenotypic evolution and further elucidate the genetic control of monotreme stomach anatomy and physiology.

evolutionary biology↗

Relationship between weapon size and six key behavioural and physiological traits in males of the European earwig

In many animals, male weapons are large and extravagant morphological structures that typically enhance fighting ability and reproductive success. It is generally assumed that growing and carrying large weapons is costly, thus only males in the best condition can afford it. In the European earwig, males carry weapons in the form of forceps-like cerci, which can vary widely in size within populations. While long forceps appear to increase males access to females, it is unknown whether it also correlates with other important male lifen-history traits. This information is important, however, in determining the potential reliability of forceps length as an indicator of male quality and the stability of this signalling system. Here, we tested whether forceps length is associated with six important behavioural and physiological traits in males of the European earwig. We sampled hundreds of males from two populations, selected 60 males with the longest and shortest forceps from each population, and then measured locomotor performance, boldness, aggregation behaviour, survival under harsh conditions, sperm storage, and survival after pathogen exposure. Contrary to our predictions, we detected no main association between forceps length and the traits measured. This lack of association was consistent between the two populations, although there were population-specific levels of boldness, aggregation and survival in harsh conditions (for long-forceps males only). Overall, these results challenge our current understanding of the function and quality signal of forceps length in this species and raise questions about the evolutionary drivers that could explain the maintenance of weapon size diversity within and between populations.

evolutionary biology↗