Whole genomes from the extinct Xerces Blue butterfly can help identify declining insect species.

The Xerces Blue (Glaucopsyche xerces) is considered to be the first butterfly to become extinct in historical times. It was notable for its chalky lavender wings with conspicuous white spots on the ventral wings. The last individuals were collected in their restricted habitat, in the dunes near the Presidio military base in San Francisco, in 1941. We sequenced the genomes of four 80- to 100-year-old Xerces Blue, and seven historical and one modern specimens of its closest relative, the Silvery Blue (Glaucopsyche lygdamus). We compared these to a novel annotated genome of the Green-Underside Blue (Glaucopsyche alexis). Phylogenetic relationships inferred from complete mitochondrial genomes indicate that Xerces Blue was a distinct species that diverged from the Silvery Blue lineage at least 850,000 years ago. Using nuclear genomes, both species experienced population growth during the Eemian interglacial period, but the Xerces Blue decreased to a very low effective population size subsequently, a trend opposite to that observed in the Silvery Blue. Runs of homozygosity and deleterious load in the former were significantly greater than in the later, suggesting a higher incidence of inbreeding. These signals of population decline observed in Xerces Blue could be used to identify and monitor other insects threatened by human activities, whose extinction patterns are still not well known.

Alasemenia, the earliest ovule with three wings and without cupule.

The ovules or seeds (fertilized ovules) with wings are widespread and especially important for wind dispersal. However, the earliest ovules in the Famennian of the Late Devonian are rarely known about the dispersal syndrome and usually surrounded by a cupule. From Xinhang, Anhui, China, we now report a new taxon of Famennian ovules, Alasemenia tria gen. et sp. nov. Each ovule of this taxon possesses three integumentary wings evidently extending outwards, folding inwards along abaxial side and enclosing most part of nucellus. The ovule is borne terminally on smooth dichotomous branches and lacks a cupule. Alasemenia suggests that the integuments of the earliest ovules without a cupule evolved functions in probable photosynthetic nutrition and wind dispersal. It indicates that the seed wing originated earlier than other wind dispersal mechanisms such as seed plume and pappus, and that three- or four-winged seeds were followed by seeds with less wings. Mathematical analysis shows that three-winged seeds are more adapted to wind dispersal than seeds with one, two or four wings under the same condition.

Many plants need seeds to reproduce. Seeds come in all shapes and sizes and often have extra features that help them disperse in the environment. For example, some seeds develop wings from seed coat as an outer layer, similar to fruits of sycamore trees that have two wings to help them glide in the wind. The first seeds are thought to have evolved around 372-359 million years ago in a period known as the Famennian (belonging to the Late Devonian). Fossil records indicate that almost all these seeds were surrounded by an additional protective structure known as the cupule and did not have wings. To date, only two groups of Famennian seeds have been reported to bear wings or wing-like structures, and one of these groups did not have cupules. These Famennian seeds all had four wings. Wang et al. examined fossils of seed plants collected in Anhui province, China, which date to the Famennian period. The team identified a new group of seed plants named the Alasemenia genus. The seeds of these plants each had three wings but no cupules. The seeds formed on branches that did not have any leaves, which indicates the seeds may have performed photosynthesis (the process by which plants generate energy from sunlight). Mathematical modelling suggested that these three-winged seeds were better adapted to being dispersed by the wind than other seeds with one, two or four wings. These findings suggest that during the Famennian the outer layer of some seeds that lacked cupules evolved wings to help the seeds disperse in the wind. It also indicates that seeds with four or three wings evolved first, followed by other groups of seed plants with fewer seed wings. Future studies may find more winged seeds and further our understanding of their evolutionary roles in the early history of seed plants.

Multiple origins of dorsal ecdysial sutures in trilobites and their relatives.

Euarthropods are an extremely diverse phylum in the modern, and have been since their origination in the early Palaeozoic. They grow through moulting the exoskeleton (ecdysis) facilitated by breaking along lines of weakness (sutures). Artiopodans, a group that includes trilobites and their non-biomineralizing relatives, dominated arthropod diversity in benthic communities during the Palaeozoic. Most trilobites - a hyperdiverse group of tens of thousands of species - moult by breaking the exoskeleton along cephalic sutures, a strategy that has contributed to their high diversity during the Palaeozoic. However, the recent description of similar sutures in early diverging non-trilobite artiopodans means that it is unclear whether these sutures evolved deep within Artiopoda, or convergently appeared multiple times within the group. Here, we describe new well-preserved material of Acanthomeridion, a putative early diverging artiopodan, including hitherto unknown details of its ventral anatomy and appendages revealed through CT scanning, highlighting additional possible homologous features between the ventral plates of this taxon and trilobite free cheeks. We used three coding strategies treating ventral plates as homologous to trilobite-free cheeks, to trilobite cephalic doublure, or independently derived. If ventral plates are considered homologous to free cheeks, Acanthomeridion is recovered sister to trilobites, however, dorsal ecdysial sutures are still recovered at many places within Artiopoda. If ventral plates are considered homologous to doublure or non-homologous, then Acanthomeridion is not recovered as sister to trilobites, and thus the ventral plates represent a distinct feature to trilobite doublure/free cheeks.

Evolution of transmissible cancers: An adaptive, plastic strategy of selfish genetic elements?

A growing number of studies have applied evolutionary and ecological principles to understanding cancer. However, few such studies have examined whether phenotypic plasticity--the ability of a single individual or genome to respond differently to different environmental circumstances--can impact the origin and spread of cancer. Here, we propose the adaptive horizontal transmission hypothesis to explain how flexible decision-making by selfish genetic elements can cause them to spread from the genome of their original host into the genomes of other hosts through the evolution of transmissible cancers. Specifically, we hypothesize that such cancers appear when the likelihood of successful vertical transmission is sufficiently low relative to the likelihood of successful horizontal transmission. We develop an evolutionary optimization model of this hypothesis, highlight empirical findings that support it, and offer suggestions for future research. Generally, phenotypically plastic selfish genetic elements might play an important role in the evolution of transmissible cancers.

Morphological evolution and functional consequences of giantism in tyrannosauroid dinosaurs.

Tyrannosauroids are a clade of theropod dinosaur taxa that varied greatly in their body size distribution. We investigated the feeding performance of six tyrannosaur genera of variable body size and skull morphology. We used 3D finite element analysis to test whether skull shape becomes more or less resistant to feeding-induced forces. Cranial and mandibular models were scaled by adult Tyrannosaurus's surface area to analyze the influence of shape on skull function. It was found that Tyrannosaurus experienced higher absolute stresses compared to small-bodied relatives. When surface area values were equalized across genera to account for the effect of size and test efficiency of skull shape, smaller individuals experience notably greater stresses than larger relatives due to the robust cranial osteology characterized in the allometry of tyrannosaurids. These results may indicate that the wide crania of tyrannosaurids convey a functional advantage that basal tyrannosauroids, juvenile tyrannosauroids, and alioramins lacked.

Improved inference of population histories by integrating genomic and epigenomic data.

With the availability of high-quality full genome polymorphism (SNPs) data, it becomes feasible to study the past demographic and selective history of populations in exquisite detail. However, such inferences still suffer from a lack of statistical resolution for recent, for example bottlenecks, events, and/or for populations with small nucleotide diversity. Additional heritable (epi)genetic markers, such as indels, transposable elements, microsatellites, or cytosine methylation, may provide further, yet untapped, information on the recent past population history. We extend the Sequential Markovian Coalescent (SMC) framework to jointly use SNPs and other hyper-mutable markers. We are able to (1) improve the accuracy of demographic inference in recent times, (2) uncover past demographic events hidden to SNP-based inference methods, and (3) infer the hyper-mutable marker mutation rates under a finite site model. As a proof of principle, we focus on demographic inference in Arabidopsis thaliana using DNA methylation diversity data from 10 European natural accessions. We demonstrate that segregating single methylated polymorphisms (SMPs) satisfy the modeling assumptions of the SMC framework, while differentially methylated regions (DMRs) are not suitable as their length exceeds that of the genomic distance between two recombination events. Combining SNPs and SMPs while accounting for site- and region-level epimutation processes, we provide new estimates of the glacial age bottleneck and post-glacial population expansion of the European A. thaliana population. Our SMC framework readily accounts for a wide range of heritable genomic markers, thus paving the way for next-generation inference of evolutionary history by combining information from several genetic and epigenetic markers.

Distinguishing mutants that resist drugs via different mechanisms by examining fitness tradeoffs.

There is growing interest in designing multidrug therapies that leverage tradeoffs to combat resistance. Tradeoffs are common in evolution and occur when, for example, resistance to one drug results in sensitivity to another. Major questions remain about the extent to which tradeoffs are reliable, specifically, whether the mutants that provide resistance to a given drug all suffer similar tradeoffs. This question is difficult because the drug-resistant mutants observed in the clinic, and even those evolved in controlled laboratory settings, are often biased towards those that provide large fitness benefits. Thus, the mutations (and mechanisms) that provide drug resistance may be more diverse than current data suggests. Here, we perform evolution experiments utilizing lineage-tracking to capture a fuller spectrum of mutations that give yeast cells a fitness advantage in fluconazole, a common antifungal drug. We then quantify fitness tradeoffs for each of 774 evolved mutants across 12 environments, finding these mutants group into classes with characteristically different tradeoffs. Their unique tradeoffs may imply that each group of mutants affects fitness through different underlying mechanisms. Some of the groupings we find are surprising. For example, we find some mutants that resist single drugs do not resist their combination, while others do. And some mutants to the same gene have different tradeoffs than others. These findings, on one hand, demonstrate the difficulty in relying on consistent or intuitive tradeoffs when designing multidrug treatments. On the other hand, by demonstrating that hundreds of adaptive mutations can be reduced to a few groups with characteristic tradeoffs, our findings may yet empower multidrug strategies that leverage tradeoffs to combat resistance. More generally speaking, by grouping mutants that likely affect fitness through similar underlying mechanisms, our work guides efforts to map the phenotypic effects of mutation.

Mutations in an organism's DNA make the individual more likely to survive and reproduce in its environment, passing on its mutations to the next generation. Mutations can alter the proteins that a gene codes for in many ways. This leads to a situation where seemingly similar mutations ­ such as two mutations in the same gene ­ can have different effects. For example, two different mutations could affect the primary function of the encoded protein in the same way but have different side effects. One mutation might also cause the protein to interact with a new molecule or protein. Organisms possessing one or the other mutation will thus have similar odds of surviving and reproducing in some environments, but differences in environments where the new interaction is important. In microorganisms, mutations can lead to drug resistance. If drug-resistant mutations have different side effects, it can be challenging to treat microbial infections, as drug-resistant pathogens are often treated with sequential drug strategies. These strategies rely on mutations that cause resistance to the first drug all having susceptibility to the second drug. But if similar seeming mutations can have diverse side effects, predictions about how they will respond to a second drug are more complicated. To address this issue, Schmidlin, Apodaca et al. collected a diverse group of nearly a thousand mutant yeast strains that were resistant to a drug called fluconazole. Next, they asked to what extent the fitness ­ the ability to survive and reproduce ­ of these mutants responded similarly to environmental change. They used this information to cluster mutations into groups that likely have similar effects at the molecular level, finding at least six such groups with unique trade-offs across environments. For example, some groups resisted only low drug concentrations, and others were unique in that they resisted treatment with two single drugs but not their combination. These diverse types of fluconazole-resistant yeast lineages highlight the challenges of designing a simple sequential drug treatment that targets all drug-resistant mutants. However, the results also suggest some predictability in how drug-resistant infections can evolve and be treated.

The genetic architecture of the load linked to dominant and recessive self-incompatibility alleles in Arabidopsis halleri and Arabidopsis lyrata.

The long-term balancing selection acting on mating types or sex-determining genes is expected to lead to the accumulation of deleterious mutations in the tightly linked chromosomal segments that are locally 'sheltered' from purifying selection. However, the factors determining the extent of this accumulation are poorly understood. Here, we took advantage of variations in the intensity of balancing selection along a dominance hierarchy formed by alleles at the sporophytic self-incompatibility system of the Brassicaceae to compare the pace at which linked deleterious mutations accumulate among them. We first experimentally measured the phenotypic manifestation of the linked load at three different levels of the dominance hierarchy. We then sequenced and phased polymorphisms in the chromosomal regions linked to 126 distinct copies of S-alleles in two populations of Arabidopsis halleri and three populations of Arabidopsis lyrata. We find that linkage to the S-locus locally distorts phylogenies over about 10-30 kb along the chromosome. The more intense balancing selection on dominant S-alleles results in greater fixation of linked deleterious mutations, while recessive S-alleles accumulate more linked deleterious mutations that are segregating. Hence, the structure rather than the overall magnitude of the linked genetic load differs between dominant and recessive S-alleles. Our results have consequences for the long-term evolution of new S-alleles, the evolution of dominance modifiers between them, and raise the question of why the non-recombining regions of some sex and mating type chromosomes expand over evolutionary times while others, such as the S-locus of the Brassicaceae, remain restricted to small chromosomal regions.

The protein domains of vertebrate species in which selection is more effective have greater intrinsic structural disorder.

The nearly neutral theory of molecular evolution posits variation among species in the effectiveness of selection. In an idealized model, the census population size determines both this minimum magnitude of the selection coefficient required for deleterious variants to be reliably purged, and the amount of neutral diversity. Empirically, an 'effective population size' is often estimated from the amount of putatively neutral genetic diversity and is assumed to also capture a species' effectiveness of selection. A potentially more direct measure of the effectiveness of selection is the degree to which selection maintains preferred codons. However, past metrics that compare codon bias across species are confounded by among-species variation in %GC content and/or amino acid composition. Here, we propose a new Codon Adaptation Index of Species (CAIS), based on Kullback-Leibler divergence, that corrects for both confounders. We demonstrate the use of CAIS correlations, as well as the Effective Number of Codons, to show that the protein domains of more highly adapted vertebrate species evolve higher intrinsic structural disorder.

Evolution is the process through which populations change over time, starting with mutations in the genetic sequence of an organism. Many of these mutations harm the survival and reproduction of an organism, but only by a very small amount. Some species, especially those with large populations, can purge these slightly harmful mutations more effectively than other species. This fact has been used by the 'drift barrier theory' to explain various profound differences amongst species, including differences in biological complexity. In this theory, the effectiveness of eliminating slightly harmful mutations is specified by an 'effective' population size, which depends on factors beyond just the number of individuals in the population. Effective population size is normally calculated from the amount of time a 'neutral' mutation (one with no effect at all) stays in the population before becoming lost or taking over. Estimating this time requires both representative data for genetic diversity and knowledge of the mutation rate. A major limitation is that these data are unavailable for most species. A second limitation is that a brief, temporary reduction in the number of individuals has an oversized impact on the metric, relative to its impact on the number of slighly harmful mutations accumulated. Weibel, Wheeler et al. developed a new metric to more directly determine how effectively a species purges slightly harmful mutations. Their approach is based on the fact that the genetic code has 'synonymous' sequences. These sequences code for the same amino acid building block, with one of these sequences being only slightly preferred over others. The metric by Weibel, Wheeler et al. quantifies the proportion of the genome from which less preferred synonymous sequences have been effectively purged. It judges a population to have a higher effective population size when the usage of synonymous sequences departs further from the usage predicted from mutational processes. The researchers expected that natural selection would favour 'ordered' proteins with robust three-dimensional structures, i.e., that species with a higher effective population size would tend to have more ordered versions of a protein. Instead, they found the opposite: species with a higher effective population size tend to have more disordered versions of the same protein. This changes our view of how natural selection acts on proteins. Why species are so different remains a fundamental question in biology. Weibel, Wheeler et al. provide a useful tool for future applications of drift barrier theory to a broad range of ways that species differ.

Protocol for high-resolution 3D visualization of insect regenerating legs through micro-computed tomography.

Appendage regeneration occurs within the opaque exoskeleton in arthropods, making it challenging to visualize the regenerative processes dynamically. In this protocol, we present a strategy to scan and capture the high-resolution details of microstructural tissues at certain regeneration points through micro-computed tomography (micro-CT). We describe steps for tissue preparation, fixation, critical point drying, micro-CT scanning, and 3D visualization. This approach promises significant utility in the field of regeneration, particularly in studies involving arthropods such as insects and crustaceans. For complete details on the use and execution of this protocol, please refer to Ren et al.1.

Reversions mask the contribution of adaptive evolution in microbiomes.

When examining bacterial genomes for evidence of past selection, the results depend heavily on the mutational distance between chosen genomes. Even within a bacterial species, genomes separated by larger mutational distances exhibit stronger evidence of purifying selection as assessed by dN/dS, the normalized ratio of nonsynonymous to synonymous mutations. Here, we show that the classical interpretation of this scale dependence, weak purifying selection, leads to problematic mutation accumulation when applied to available gut microbiome data. We propose an alternative, adaptive reversion model with opposite implications for dynamical intuition and applications of dN/dS. Reversions that occur and sweep within-host populations are nearly guaranteed in microbiomes due to large population sizes, short generation times, and variable environments. Using analytical and simulation approaches, we show that adaptive reversion can explain the dN/dS decay given only dozens of locally fluctuating selective pressures, which is realistic in the context of Bacteroides genomes. The success of the adaptive reversion model argues for interpreting low values of dN/dS obtained from long timescales with caution as they may emerge even when adaptive sweeps are frequent. Our work thus inverts the interpretation of an old observation in bacterial evolution, illustrates the potential of mutational reversions to shape genomic landscapes over time, and highlights the importance of studying bacterial genomic evolution on short timescales.

Conserved signaling modules regulate filamentous growth in fungi: a model for eukaryotic cell differentiation.

Eukaryotic organisms are composed of different cell types with defined shapes and functions. Specific cell types are produced by the process of cell differentiation, which is regulated by signal transduction pathways. Signaling pathways regulate cell differentiation by sensing cues and controlling the expression of target genes whose products generate cell types with specific attributes. In studying how cells differentiate, fungi have proved valuable models because of their ease of genetic manipulation and striking cell morphologies. Many fungal species undergo filamentous growth-a specialized growth pattern where cells produce elongated tube-like projections. Filamentous growth promotes expansion into new environments, including invasion into plant and animal hosts by fungal pathogens. The same signaling pathways that regulate filamentous growth in fungi also control cell differentiation throughout eukaryotes and include highly conserved mitogen-activated protein kinase (MAPK) pathways, which is the focus of this review. In many fungal species, mucin-type sensors regulate MAPK pathways to control filamentous growth in response to diverse stimuli. Once activated, MAPK pathways reorganize cell polarity, induce changes in cell adhesion, and promote the secretion of degradative enzymes that mediate access to new environments. However, MAPK pathway regulation is complicated because related pathways can share components with each other yet induce unique responses (i.e. signal specificity). In addition, MAPK pathways function in highly integrated networks with other regulatory pathways (i.e. signal integration). Here, we discuss signal specificity and integration in several yeast models (mainly Saccharomyces cerevisiae and Candida albicans) by focusing on the filamentation MAPK pathway. Because of the strong evolutionary ties between species, a deeper understanding of the regulation of filamentous growth in established models and increasingly diverse fungal species can reveal fundamentally new mechanisms underlying eukaryotic cell differentiation.

A hybrid biosynthetic-catabolic pathway for norspermidine production.

The only known pathway for biosynthesis of the polyamine norspermidine starts from aspartate ß-semialdehyde to form the diamine 1,3-diaminopropane, which is then converted to norspermidine via a carboxynorspermidine intermediate. This pathway is found primarily in the Vibrionales order of the γ-Proteobacteria. However, norspermidine is also found in other species of bacteria and archaea, and in diverse single-celled eukaryotes, chlorophyte algae and plants that do not encode the known norspermidine biosynthetic pathway. We reasoned that products of polyamine catabolism could be an alternative route to norspermidine production. 1,3-diaminopropane is formed from terminal catabolism of spermine and spermidine, and norspermidine can be formed from catabolism of thermospermine. We found that the single-celled chlorophyte alga Chlamydomonas reinhardtii thermospermine synthase (CrACL5) did not aminopropylate exogenously-derived 1,3-diaminopropane efficiently when expressed in Escherichia coli. In contrast, it completely converted all E. coli native spermidine to thermospermine. Co-expression in E. coli of the polyamine oxidase 5 from lycophyte plant Selaginella lepidophylla (SelPAO5), together with the CrACL5 thermospermine synthase, converted almost all thermospermine to norspermidine. Although CrACL5 was efficient at aminopropylating norspermidine to form tetraamine norspermine, SelPAO5 oxidizes norspermine back to norspermidine, with the balance of flux being inclined fully to norspermine oxidation. The steady-state polyamine content of E. coli co-expressing thermospermine synthase CrACL5 and polyamine oxidase SelPAO5 was an almost total replacement of spermidine by norspermidine. We have recapitulated a potential hybrid biosynthetic-catabolic pathway for norspermidine production in E. coli, which could explain norspermidine accumulation in species that do not encode the known aspartate ß-semialdehyde-dependent pathway.

An arms race between 5'ppp-RNA virus and its alternative recognition receptor MDA5 in RIG-I-lost teleost fish.

The incessant arms race between viruses and hosts has led to numerous evolutionary innovations that shape life's evolution. During this process, the interactions between viral receptors and viruses have garnered significant interest since viral receptors are cell surface proteins exploited by viruses to initiate infection. Our study sheds light on the arms race between the MDA5 receptor and 5'ppp-RNA virus in a lower vertebrate fish, Miichthys miiuy. Firstly, the frequent and independent loss events of RIG-I in vertebrates prompted us to search for alternative immune substitutes, with homology-dependent genetic compensation response (HDGCR) being the main pathway. Our further analysis suggested that MDA5 of M. miiuy and Gallus gallus, the homolog of RIG-I, can replace RIG-I in recognizing 5'ppp-RNA virus, which may lead to redundancy of RIG-I and loss from the species genome during evolution. Secondly, as an adversarial strategy, 5'ppp-RNA SCRV can utilize the m6A methylation mechanism to degrade MDA5 and weaken its antiviral immune ability, thus promoting its own replication and immune evasion. In summary, our study provides a snapshot into the interaction and coevolution between vertebrate and virus, offering valuable perspectives on the ecological and evolutionary factors that contribute to the diversity of the immune system.

Before the immune system can eliminate a bacterium, virus or other type of pathogen, it needs to be able to recognize these foreign elements. To achieve this, cells in the immune system have proteins called pattern recognition receptors (PRRs) which can identify distinct molecular features of certain pathogens. One specific group of PRRs is a family of retinoic acid-induced RIG-I-like receptors (RLRs), which help immune cells detect different types of viruses. Members of this family recognize distinct motifs on the genetic material of viruses known as RNA. For instance, RIG-I recognizes a marker known as 5'ppp on the end of single-stranded RNA molecules, whereas MDA5 recognizes long strands of double-stranded RNA. Many vertebrates ­ including various mammals, birds, and fish ­ lost the RIG-I receptor over the course of evolution. However, Geng et al. predicted that some animals lacking the RIG-I receptor may still be able to activate an immune response against viruses that contain the 5'ppp-RNA motif. To investigate this possibility, Geng et al. studied chickens and miiuy croakers (a type of ray-finned fish) which no longer have a RIG-I receptor. They found that both animals can still sense and eliminate two 5'ppp-RNA viruses called VSV and SCRV. Further experiments revealed that these two viruses are detected by a modified MDA5 receptor that had evolved to bind to 5'-ppp and activate the antiviral response. Viruses are also continuously evolving new ways to escape the immune system. This led Geng et al. to investigate whether SCRV, which causes serious harm to marine fish, has evolved a way to evade the MDA5 protection mechanism. Using miiuy croakers as a model, they found that SCRV causes the transcripts that produce the MDA5 protein to contain more molecules of m6a. This molecular tag degrades the transcript, leading to lower levels of MDA5, reducing the antiviral response against SCRV. The findings of Geng et al. offer valuable perspectives on how the immune system adapts over the course of evolution, and highlight the diversity of antiviral responses in vertebrates. Chickens and miiuy croakers are commonly farmed animals, and further work investigating how viruses invade these species could prevent illnesses from spreading and having a negative impact on the economy.

Neuro-evolutionary evidence for a universal fractal primate brain shape.

The cerebral cortex displays a bewildering diversity of shapes and sizes across and within species. Despite this diversity, we present a universal multi-scale description of primate cortices. We show that all cortical shapes can be described as a set of nested folds of different sizes. As neighbouring folds are gradually merged, the cortices of 11 primate species follow a common scale-free morphometric trajectory, that also overlaps with over 70 other mammalian species. Our results indicate that all cerebral cortices are approximations of the same archetypal fractal shape with a fractal dimension of df = 2.5. Importantly, this new understanding enables a more precise quantification of brain morphology as a function of scale. To demonstrate the importance of this new understanding, we show a scale-dependent effect of ageing on brain morphology. We observe a more than fourfold increase in effect size (from two standard deviations to eight standard deviations) at a spatial scale of approximately 2 mm compared to standard morphological analyses. Our new understanding may, therefore, generate superior biomarkers for a range of conditions in the future.

Many of the brain's essential functions ­ from decision-making to movement ­ take place in its outer layer known as the cerebral cortex. The shape of the cerebral cortex varies significantly between species. For instance, in humans, it is folded in to grooves and ridges, whereas in other animals, including mice, it is completely smooth. The structure of the cortex can also differ within a species, and be altered by aging and certain diseases. This vast variation can make it difficult it to characterize and compare the structure of the cortex between different species, ages and diseases. To address this, Wang et al. developed a new mathematical model for describing the shape of the cortex. The model uses a method known as coarse graining to erase, or 'melt away', any cortical folds or structures smaller than a given threshold size. As this threshold increases, the cortex becomes progressively smoother. The relationship between surface areas and threshold sizes indicates the fractal dimension ­ that is, how fragmented the cortex is across different scales. Wang et al. applied their model to the brain scans of eleven primates, including humans, and found the fractal dimension of the cortex was almost exactly 2.5 for all eleven species. This suggests that the cortices of the different primates follow a single fractal shape, which means the folds of each cortex have a similar branching pattern. Although there were distinctions between the species, they were mainly due to the different ranges of fold sizes in each cortex. The model revealed that the broader the range of fold sizes, the more folded the brain ­ but the fractal pattern remains the same. The brain melting method created by Wang et al. provides a new way to characterise cortical shape. Besides revealing a hitherto hidden regularity of nature, they hope that in the future their new method will be useful in assessing brain changes during human development and ageing, and in diseases like Alzheimer's and epilepsy.

Venom exaptation and adaptation during the trophic switch to blood-feeding by kissing bugs.

Kissing bugs are known to produce anticoagulant venom that facilitates blood-feeding. However, it is unknown how this saliva evolved and if the venom produced by the entomophagous ancestors of kissing bugs would have helped or hindered the trophic shift. In this study, we show that venoms produced by extant predatory assassin bugs have strong anticoagulant properties mediated chiefly by proteolytic degradation of fibrinogen, and additionally contain anticoagulant disulfide-rich peptides. However, venom produced by predatory species also has pain-inducing and membrane-permeabilizing activities that would be maladaptive for blood-feeding, and which venom of the blood-feeding species lack. This study demonstrates that venom produced by the predatory ancestors of kissing bugs was exapted for the trophic switch to blood-feeding by virtue of its anticoagulant properties. Further adaptation to blood-feeding occurred by downregulation of venom toxins with proteolytic, cytolytic, and pain-inducing activities, and upregulation and neofunctionalization of toxins with anticoagulant activity independent of proteolysis.

Starving infecund widow spiders maintain sexual attractiveness and trade off safety for enhanced prey capture.

Starving animals must balance their resources between immediate survival and future reproduction. False widow spiders, Steatoda grossa, inhabit indoor settings with scarce prey. Here, we investigated the effects of lengthy starvation on the physiology, web architecture, sexual signaling, and reproductive success of S. grossa females. Compared to well-fed females, starving females (1) lost body mass faster, (2) had lower survival, (3) produced more silk for prey capture than for safety, and (4) deposited less contact pheromone components on their webs but accelerated their hydrolysis to mate-attractant components. As starving females became infecund - but still attracted and copulated with males - they misguided males that would gain reproductive fitness by selecting fecund females. Whether starving females store sperm and potentially regain fecundity upon feeding is still unknown. Our study shows how prey shortage shapes sexual signaling, predation, and reproductive behavior of S. grossa females that seem to engage in deceptive signaling.

Protocol for measuring the effects of an inhibitory signal associated with danger on honey bee dopamine levels.

The stop signal is produced in response to negative experiences at the food source and inhibits honey bee (Apis mellifera) waggle dancing. Here, we present a protocol for measuring the effects of an inhibitory signal associated with danger on honey bee dopamine levels. We describe steps for observing honey bee colonies, training them with artificial nectar, and simulating hornet attacks. We then detail procedures for recording waggle dancing and stop signals and measuring brain dopamine levels during different treatments. For complete details on the use and execution of this protocol, please refer to Dong et al.1.

Recent evolutionary origin and localized diversity hotspots of mammalian coronaviruses.

Several coronaviruses infect humans, with three, including the SARS-CoV2, causing diseases. While coronaviruses are especially prone to induce pandemics, we know little about their evolutionary history, host-to-host transmissions, and biogeography. One of the difficulties lies in dating the origination of the family, a particularly challenging task for RNA viruses in general. Previous cophylogenetic tests of virus-host associations, including in the Coronaviridae family, have suggested a virus-host codiversification history stretching many millions of years. Here, we establish a framework for robustly testing scenarios of ancient origination and codiversification versus recent origination and diversification by host switches. Applied to coronaviruses and their mammalian hosts, our results support a scenario of recent origination of coronaviruses in bats and diversification by host switches, with preferential host switches within mammalian orders. Hotspots of coronavirus diversity, concentrated in East Asia and Europe, are consistent with this scenario of relatively recent origination and localized host switches. Spillovers from bats to other species are rare, but have the highest probability to be towards humans than to any other mammal species, implicating humans as the evolutionary intermediate host. The high host-switching rates within orders, as well as between humans, domesticated mammals, and non-flying wild mammals, indicates the potential for rapid additional spreading of coronaviruses across the world. Our results suggest that the evolutionary history of extant mammalian coronaviruses is recent, and that cases of long-term virus-host codiversification have been largely over-estimated.

The SARS-CoV-2 virus, which caused the recent global coronavirus pandemic, is the latest in a string of coronaviruses that have caused serious outbreaks. This group of coronaviruses can also infect other mammals and likely jumped between species ­ including from non-humans to humans ­ over the course of evolution. Determining when and how viruses evolved to infect humans can help scientists predict and prevent outbreaks. However, tracking the evolutionary trajectory of coronaviruses is challenging, and there are conflicting views on how often coronaviruses crossed between species and when these transitions likely occurred. Some studies suggest that coronaviruses originated early on in evolution and evolved together with their mammalian hosts, only occasionally jumping to and from different species. While others suggest they appeared more recently, and rapidly diversified by regularly transferring between species. To determine which is the most likely scenario, Maestri, Perez-Lamarque et al. developed a computational approach using already available data on the genetics and evolutionary history of mammals and coronaviruses. This revealed that coronaviruses originated recently in bats from East Asia and Europe, and primarily evolved by rapidly transferring between different mammalian species. This has led to geographical hotspots of diverse coronaviruses in East Asia and Europe. Maestri, Perez-Lamarque et al. found that it was rare for coronaviruses to spill over from bats to other types of mammals. Most of these spillovers resulted from coronaviruses jumping from bats to humans or domesticated animals. Humans appeared to be the main intermediary host that coronaviruses temporarily infected as they transferred from bats to other mammals. These findings ­ that coronaviruses emerged recently in evolution, jumped relatively frequently between species, and are geographically restricted ­ suggest that future transmissions are likely. Gathering more coronavirus samples from across the world and using even more powerful analysis tools could help scientists understand more about how these viruses recently evolved. These insights may lead to strategies for preventing new coronaviruses from emerging and spreading among humans.