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Plants have numerous mechanisms to cope with the negative effects of herbivory, including plant resistance, structural and chemical traits that reduce damage, and plant tolerance, the ability to compensate for tissues lost. It has been argued that resistance and tolerance represent alternate strategies and thus there should be a trade-off between resistance and tolerance. However, resistance and tolerance are controlled via the same molecular pathway, the oxidative pentose phosphate pathway and the process of endoreduplication. Endoreduplication is the replication of the genome without mitosis, which leads to an increase in cellular chromosome number. Increasing chromosome number and therefore gene copy number provides a means of increasing gene expression that has been shown to enhance compensation following herbivory. By measuring glucosinolate levels and seed production following the removal of apical dominance in genotypes of Arabidopsis thaliana we show that there is a positive association between tolerance and induced chemical defense. Similarly, the direct association between tolerance and resistance is demonstrated by genetically manipulating the endoreduplication pathway. By overexpressing ILP1, a positive regulator of endoreduplication, and thus compensation, we experimentally increased glucosinolate production and tolerance in the Col-0 genotype. We suggest that many herbaceous plants that endoreduplicate (∼90%) would show a positive relationship between compensation and chemical defense, given that the molecular pathways are shared in common. We discuss these findings in light of contrasting results on measures of tolerance and resistance, given that the true relationship can be masked by ignoring genetic variation in endoreduplication and the timing of chemical measurement.

Utilizing geochemical analysis, this study identifies the sources of European brass used in the casting of the renowned Benin Bronzes, produced by the Edo people of Nigeria. It is commonly believed that distinctive brass rings known as “manillas”, used as currency in the European trade in West Africa, also served as a metal source for the making of the Bronzes. However, prior to the current study, no research had conclusively connected the Benin artworks and the European manillas. For this research, manillas from shipwrecks in African, American and European waters dating between the 16th and 19th Century were analysed using ICP-MS analysis. Comparing trace elements and lead isotope ratios of manillas and Benin Bronzes identifies Germany as the principal source of the manillas used in the West African trade between the 15 th and 18 th centuries before British industries took over the brass trade in the late 18 th century.

That some plants benefit from being eaten is counterintuitive, yet there is now considerable evidence demonstrating enhanced fitness following herbivory (i.e., plants can overcompensate). Although there is evidence that genetic variation for compensation exists, little is known about the genetic mechanisms leading to enhanced growth and reproduction following herbivory. We took advantage of the compensatory variation in recombinant inbred lines of Arabidopsis thaliana, combined with microarray and QTL analyses to assess the molecular basis of overcompensation. We found three QTL explaining 11.4, 10.1, and 26.7% of the variation in fitness compensation, respectively, and 109 differentially expressed genes between clipped and unclipped plants of the overcompensating ecotype Columbia. From the QTL/microarray screen we uncovered one gene that plays a significant role in overcompensation: glucose-6-phosphate-1-dehydrogenase (G6PDH1). Knockout studies of Transfer-DNA (T-DNA) insertion lines and complementation studies of G6PDH1 verify its role in compensation. G6PDH1 is a key enzyme in the oxidative pentose-phosphate pathway that plays a central role in plant metabolism. We propose that plants capable of overcompensating reprogram their transcriptional activity by up-regulating defensive genes and genes involved in energy metabolism and by increasing DNA content (via endoreduplication) with the increase in DNA content feeding back on pathways involved in defense and metabolism through increased gene expression.

Viral respiratory infections are an important public health concern due to their prevalence, transmissibility, and potential to cause serious disease. Disease severity is the product of several factors beyond the presence of the infectious agent, including specific host immune responses, host genetic makeup, and bacterial coinfections. To understand these interactions within natural infections, we designed a longitudinal cohort study actively surveilling respiratory viruses over the course of 19 months (2016 to 2018) in a diverse cohort in New York City. We integrated the molecular characterization of 800+ nasopharyngeal samples with clinical data from 104 participants. Transcriptomic data enabled the identification of respiratory pathogens in nasopharyngeal samples, the characterization of markers of immune response, the identification of signatures associated with symptom severity, individual viruses, and bacterial coinfections. Specific results include a rapid restoration of baseline conditions after infection, significant transcriptomic differences between symptomatic and asymptomatic infections, and qualitatively similar responses across different viruses. We created an interactive computational resource (Virome Data Explorer) to facilitate access to the data and visualization of analytical results.

Herbivory is a fundamental type of plant–animal interaction that presents substantial selection pressure on plants to replace lost tissues and to prevent subsequent losses in fitness. Apical herbivory, which entails removal or damage to the apical meristem, causes a change in plant architecture by disrupting the balance of hormones produced in part by the apical meristem. Therefore, for an annual semelparous plant, the ability to preserve reproductive success following damage (i.e., to tolerate damage) is largely dependent on the plant’s pre-damage investment into fitness and its regrowth pattern following damage. Using multiple regression analyses, we assessed the relationship of developmental and architectural traits of experimentally damaged plants relative to undamaged plants of 33 Arabidopsis thaliana genotypes that display a wide range of undamaged fitness and damage tolerance. Our analyses revealed evidence for an evolutionary bet-hedging strategy within a subset of genotypes to presumably maximize fitness under natural herbivory—genotypes with the greatest seed production when undamaged exhibited a significant reduction in seed yield when damaged, while genotypes with low undamaged seed production were the only genotypes whose seed yield increased when damaged. Patterns of endopolyploidy paralleled those of seed production, such that the increase in whole-plant ploidy by genome re-replication during growth/regrowth contributes to undamaged fitness, damage tolerance, and their trade-off. Overall, this study provides the first large-scale characterization of A. thaliana regrowth patterns and suggests that investment into fitness and endopolyploidy when undamaged may come at a cost to tolerance ability once damaged.

Endoreduplication, the replication of the genome without mitosis, leads to endopolyploidy, an increase in cellular chromosome number. Although endoreduplication is widespread among angiosperms and other groups of eukaryotes, the degree to which this process is plastic under varying environmental conditions and its potential adaptive significance are not known. Here, using flow cytometry, we measured plasticity in chromosome number following the removal of apical dominance (simulating natural herbivory) in two ecotypes of Arabidopsis thaliana: Columbia and Landsberg erecta. We report that endopolyploidy of clipped Columbia plants was significantly different than unclipped controls following the removal of apical dominance and regrowth, and that cellular ploidy is positively associated with attributes of fitness (biomass, flower, fruit, and seed production). In contrast, clipped Landsberg erecta showed no significant differences in endopolyploidy and a decrease in seed production compared to unclipped controls; representing a significant genotype × environment interaction between ecotypes. Altering ploidy via endoreduplication adds a previously unknown way in which plants may be able to cope with environmental stress: enhancing regrowth rates and fitness following plant damage.

The work uses a well‐characterized model for predicting the dynamics of virus infections based on studies of the dynamics of influenza virus infections in humans. 4,5 After fitting the model to data from 13 hospitalized patients in Singapore to understand viral replication in the absence of treatment, they then simulated outcomes for a range of therapies considering both antiviral potency and the timing of treatment initiation. According to their data, this timing was chosen as it corresponded to typical peak viral load in the absence of treatment. Because nearly all of the target cell pool rapidly becomes infected in the model, the authors find that putative treatments blocking an early stage of the viral lifecycle (e.g., hydroxychloroquine) must be delivered at or before symptom onset to provide benefit.

While one may expect the loss of plant tissue by animal herbivores to be universally detrimental to a plant's fitness, a wide range of tolerance responses exists, including undercompensation (lower fitness when damaged), equal compensation, and even overcompensation (increased fitness when damaged). Theory predicts that these responses could be constrained by the investment into defensive chemicals and structures produced for improving resistance in damaged tissues, and thus tolerance and induced defense could be considered alternative strategies to the selection pressure imposed by herbivory. To determine which genetic pathways underlie differences in compensatory (i.e., growth and fitness) responses to damage by tissue loss, and to test their relation with pathways involved in defense, we performed a controlled greenhouse study to measure total gene expression via RNA-sequencing of undamaged and mechanically damaged plants of three Arabidopsis thaliana genotypes that differ in their compensatory performances: Columbia-4, Landsberg erecta, and a recombinant inbred line (RIL) from a Columbia-4 × Landsberg erecta cross. Among the many genetic pathways that responded to clipping, Columbia-4 significantly up-regulated genes involved in secondary defense chemistry and equally compensated for fitness while Landsberg erecta and the RIL both undercompensated and significantly down-regulated secondary defense pathways. The genotypes' different compensatory performances are thus positively correlated with their differential investments into secondary metabolism following tissue loss. This study identifies differential post-damage gene regulation of growth, developmental signaling, and environmental response pathways in A. thaliana, and provides the first transcriptomic evidence counter to the presumed tradeoff between tolerance and defense in plant-herbivore interactions.

Herbivory imposes substantial selection pressure on plants, with the ability to regrow and maintain reproductive success a challenging but often necessary response by the plant. Despite the commonness of herbivore-induced damage, vast variation in tolerance ability exists among plants. Recent studies have suggested the role of endoreduplication (increasing ploidy within an individual) and the pentose phosphate pathway (a metabolic pathway that supports both primary and secondary metabolism) in contributing to the variation in tolerance ability among genotypes of Arabidopsis thaliana. We measured natural variation in apical meristem damage frequency, endoreduplication, and the sequence of G6PD1, an important gene in the pentose phosphate pathway, and related them to variation in tolerance of natural populations of A. thaliana over a portion of its native European range. Variation among populations in tolerance was significantly positively related to damage frequency, suggesting the potential for directional selection for tolerance ability as a product of damage frequency. We also discovered likely loss-of-function G6PD1 alleles in two populations, both of which displayed among the lowest levels of tolerance of all populations assessed. In addition, populations with the greatest increase in endopolyploidy also had the greatest ability to tolerate damage while populations with the greatest reduction in endopolyploidy had the lowest ability to tolerate damage. This study provides an assessment of variation in tolerance, damage frequency, G6PD1 sequence, and endopolyploidy in natural populations of A. thaliana, and also contributes to the growing body of research on the contributions of these specific molecular mechanisms to the tolerance response.

The mutation rate of an organism is itself evolvable. In stable environments, if faithful replication is costless, theory predicts that mutation rates will evolve to zero. However, positive mutation rates can evolve in novel or fluctuating environments, as analytical and empirical studies have shown. Previous work on this question has focused on environments that fluctuate independently of the evolving population. Here we consider fluctuations that arise from frequency-dependent selection in the evolving population itself. We investigate how the dynamics of competing traits can induce selective pressure on the rates of mutation between these traits. To address this question, we introduce a theoretical framework combining replicator dynamics and adaptive dynamics. We suppose that changes in mutation rates are rare, compared to changes in the traits under direct selection, so that the expected evolutionary trajectories of mutation rates can be obtained from analysis of pairwise competition between strains of different rates. Depending on the nature of frequency-dependent trait dynamics, we demonstrate three possible outcomes of this competition. First, if trait frequencies are at a mutation–selection equilibrium, lower mutation rates can displace higher ones. Second, if trait dynamics converge to a heteroclinic cycle—arising, for example, from “rock-paper-scissors” interactions—mutator strains succeed against non-mutators. Third, in cases where selection alone maintains all traits at positive frequencies, zero and nonzero mutation rates can coexist indefinitely. Our second result suggests that relatively high mutation rates may be observed for traits subject to cyclical frequency-dependent dynamics.