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In diverse organisms, nanostructures that coherently scatter light create structural color, but how such structures are built remains mysterious. We investigate the evolution and genetic regulation of butterfly scale laminae, which are simple photonic nanostructures. In a lineage of buckeye butterflies artificially selected for blue wing color, we found that thickened laminae caused a color shift from brown to blue. Deletion of the optix patterning gene also altered color via lamina thickening, revealing shared regulation of pigments and lamina thickness. Finally, we show how lamina thickness variation contributes to the color diversity that distinguishes sexes and species throughout the genus Junonia. Thus, quantitatively tuning one dimension of scale architecture facilitates both the microevolution and macroevolution of a broad spectrum of hues. Because the lamina is an intrinsic component of typical butterfly scales, our findings suggest that tuning lamina thickness is an available mechanism to create structural color across the Lepidoptera. From iridescent blues to vibrant purples, many butterflies display dazzling ‘structural colors’ created not by pigments but by microscopic structures that interfere with light. For instance, the scales that coat their wings can contain thin films of chitin, the substance that normally makes the external skeleton of insects. In slim layers, however, chitin can also scatter light to produce color, the way that oil can create iridescence at the surface of water. The thickness of the film, which is encoded by the genes of the butterfly, determines what color will be produced. Yet, little is known about how common thin films are in butterflies, exactly how genetic information codes for them, and how their thickness and the colors they produce can evolve. To investigate, Thayer et al. used a technique called Helium Ion Microscopy and examined the wings of ten related species of butterflies, showing that thin film structures were present across this sample. However, the different species have evolved many different structural colors over the past millions of years by changing the thickness of the films. Next, Thayer et al. showed that this evolution could be reproduced at a faster pace in the laboratory using common buckeye butterflies. These insects mostly have brown wings, but they can have specks of blue created by thin film structures. Individuals with more blue on their wings were mated and over the course of a year, the thickness of the film structures increased by 74%, leading to shiny blue butterflies. Deleting a gene called optix from the insects also led to blue wings. Optix was already known to control the patterns of pigments in butterflies, but it now appears that it controls structural colors as well. From solar panels to new fabrics, microscopic structures that can scatter light are useful in a variety of industries. Understanding how these elements exist and evolve in organisms may help to better design them for human purposes.

In the past few years, huge advances have been made in techniques to analyse cells at an individual level using RNA sequencing, and many of these have precipitated exciting discoveries in the immunology of type 1 diabetes (T1D). This review will cover the first papers to use scRNAseq to characterise human lymphocyte phenotypes in T1D in the peripheral blood, pancreatic lymph nodes and islets. These have revealed specific genes such as IL-32 that are differentially expressed in islet –specific T cells in T1D. scRNAseq has also revealed wider gene expression patterns that are involved in T1D and can predict its development even predating autoantibody production. Single cell sequencing of TCRs has revealed V genes and CDR3 motifs that are commonly used to target islet autoantigens, although truly public TCRs remain elusive. Little is known about BCR repertoires in T1D, but scRNAseq approaches have revealed that insulin binding BCRs commonly use specific J genes, share motifs between donors and frequently demonstrate poly-reactivity. This review will also summarise new developments in scRNAseq technology, the insights they have given into other diseases and how they could be leveraged to advance research in the type 1 diabetes field to identify novel biomarkers and targets for immunotherapy.

In this study, a simple generic infection model was developed for predicting infection periods by fungal foliar pathogens. The model is designed primarily for use in forecasting pathogens that do not have extensive epidemiological data. Most existing infection models require a background epidemiological data set, usually including laboratory estimates of infection at multiple temperature and wetness combinations. The model developed in this study can use inputs based on subjective estimates of the cardinal temperatures and the wetness duration requirement. These inputs are available for many pathogens or may be estimated from related pathogens. The model uses a temperature response function which is scaled to the minimum and optimum values of the surface wetness duration requirement. The minimum wetness duration requirement (W(min)) is the number of hours required to produce 20% disease incidence or 5% disease severity on inoculated plant parts at a given temperature. The model was validated with published data from 53 controlled laboratory studies, each with at least four combinations of temperature and wetness. Validation yielded an average correlation coefficient of 0.83 and a root mean square error of 4.9 h, but there was uncertainty about the value of the input parameters for some pathogens. The value of W(min) varied from 1 to 48 h and was relatively uniform for species in the genera Cercospora, Alternaria, and Puccinia but less so for species of Phytophthora, Venturia, and Colletotrichum. Operationally, infection models may use hourly or daily weather inputs. In the case of the former, information also is required to estimate the critical dry-period interruption value, defined as the duration of a dry period at relative humidities <95% that will result in a 50% reduction in disease compared with a continuous wetness period. Pathogens were classified into three groups based on their critical dry-period interruption value. The infection model is being used to create risk maps of exotic pests for the U.S. Department of Agriculture's Animal Plant Health and Inspection Service.

In this study, we report a novel therapeutic approach using B lymphocytes to attract islet-specific T cells in the non-obese diabetic (NOD) mouse model and prevent the development of autoimmune diabetes. Rather than using the antibody receptor of B cells, this approach utilizes their properties as antigen-presenting cells to T cells. Purified splenic B cells were treated with lipopolysaccharide, which increases regulatory B (Breg) cell function, then electroporated with mRNA encoding either chimeric MHC-I or MHC-II molecules covalently linked to antigenic peptides. Immunoregulatory functions of these engineered B cells (e-B cells) were tested by assays and co-transfer experiments with beta-cell-antigen-specific CD8 or CD4 T cells in NOD.Scid mice, respectively. The e-B cells expressing chimeric MHC-I-peptide inhibited antigen-specific CD8 T-cell cytotoxicity . The e-B cells expressing chimeric MHC-II-peptide induced antigen-specific CD4 T cells to express the regulatory markers, PD-1, ICOS, CTLA-4, Lag3, and Nrp1. Furthermore, e-B cells encoding the chimeric MHC-I and MHC-II peptide constructs protected NOD.Scid mice from autoimmune diabetes induced by transfer of antigen-specific CD8 and CD4 T cells. MHC-peptide chimeric e-B cells interacted with pathogenic T cells, and protected the host from autoimmune diabetes, in a mouse model. Thus, we have successfully expressed MHC-peptide constructs in B cells that selectively targeted antigen-specific cells, raising the possibility that this strategy could be used to endow different protective cell types to specifically regulate/remove pathogenic cells.

Gold nanoparticles (GNPs) have been used in the development of novel therapies as a way of delivery of both stimulatory and tolerogenic peptide cargoes. Here we report that intradermal injection of GNPs loaded with the proinsulin peptide C19-A3, in patients with type 1 diabetes, results in recruitment and retention of immune cells in the skin. These include large numbers of clonally expanded T-cells sharing the same paired T-cell receptors (TCRs) with activated phenotypes, half of which, when the TCRs were re-expressed in a cell-based system, were confirmed to be specific for either GNP or proinsulin. All the identified gold-specific clones were CD8 + , whilst proinsulin-specific clones were both CD8 + and CD4 + . Proinsulin-specific CD8 + clones had a distinctive cytotoxic phenotype with overexpression of granulysin (GNLY) and KIR receptors. Clonally expanded antigen-specific T cells remained in situ for months to years, with a spectrum of tissue resident memory and effector memory phenotypes. As the T-cell response is divided between targeting the gold core and the antigenic cargo, this offers a route to improving resident memory T-cells formation in response to vaccines. In addition, our scRNAseq data indicate that focusing on clonally expanded skin infiltrating T-cells recruited to intradermally injected antigen is a highly efficient method to enrich and identify antigen-specific cells. This approach has the potential to be used to monitor the intradermal delivery of antigens and nanoparticles for immune modulation in humans.

Harmful algal blooms (HABs) can disrupt aquatic communities through a variety of mechanisms, especially through toxin production. Herbivorous and omnivorous zooplankton may be particularly susceptible to HAB toxins, due to their close trophic relationship to algae as grazers. In this study, the acute toxigenic effects of the haptophyte Prymnesium parvum on a zooplankton community were investigated under laboratory conditions. Total zooplankton abundances decreased during 48-h exposure, although species responses to P. parvum densities varied. Changes in community composition were driven by declines in Daphnia mendotae and Keratella spp. abundances, which resulted in an average shift in copepod abundance from 47.1 to 72.4%, and rotifer abundance from 35.0 to 7.1%. Total cladocerans were relatively unchanged in relative abundance (11.1–10.4%), though the dominant cladoceran shifted from Daphnia mendotae (61.3% of cladocerans) to Bosmina longirostris (81.5% of cladocerans). Daphnia mendotae and Keratella spp. are known to be non-selective or generalist feeders and were likely harmed through a combination of ingestion of and contact by P. parvum. Proportional increases in copepod and Bosmina abundances in the presence of P. parvum likely reflect selective or discriminate feeding abilities in these taxa. This study corroborates previous field studies showing that P. parvum can negatively affect zooplankton, reflecting species-specific differences in zooplankton-P. parvum interactions. Such changes can alter zooplankton community composition, leading to substantial food-web consequences and potential long-term ecosystem-level impacts in lakes that experience blooms.

Growing attention in aquatic ecology is focusing on biogeographic patterns in microorganisms and whether these potential patterns can be explained within the framework of general ecology. The long-standing microbiologist’s credo ‘Everything is everywhere, but, the environment selects’ suggests that dispersal is not limiting for microbes, but that the environment is the primary determining factor in microbial community composition. Advances in molecular techniques have provided new evidence that biogeographic patterns exist in microbes and that dispersal limitation may actually have an important role, yet more recent study using extremely deep sequencing predicts that indeed everything is everywhere. Using a long-term field study of the ‘invasive’ marine haptophyte Prymnesium parvum , we characterize the environmental niche of P. parvum in a subtropical impoundment in the southern United States. Our analysis contributes to a growing body of evidence that indicates a primary role for environmental conditions, but not dispersal, in the lake-wide abundances and seasonal bloom patterns in this globally important microbe.

Abstract Drosophila seminal fluid proteins (SFPs) are often cited as an example of interlocus sexual conflict, wherein the proteins increase male fitness while decreasing female fitness, spurring recurring female counter-adaptations and rapid molecular evolution. This model predicts that male-expressed genetic variation in the accessory gland, which produces seminal fluid, should generate counter-evolving genetic pathways in females, resulting in sexual coevolution. Using a trio of D. melanogaster populations exhibiting substantial SFP expression divergence due to recent selection, we test for coevolution in the female post-mating transcriptome in the lower reproductive tract and head. Contrasting predictions of sexual antagonism, female post-mating gene expression is indifferent to male population of origin. Instead, our results better support the alternative hypotheses that environmental variation is the source of selection on male SFP gene expression and that population differentiation in the female post-mating transcriptome is generated by female-expressed genotypic differentiation.

Existing approaches for measuring hemostasis parameters require multiple platforms, can take hours to provide results, and generally require 1-25 mL of sample. We developed a diagnostic platform that allows comprehensive assessment of hemostatic parameters on a single instrument and provides results within 15 min using 0.04 mL of blood with minimal sample handling. T2 magnetic resonance (T2MR) was used to directly measure integrated reactions in whole blood samples by resolving multiple water relaxation times from distinct sample microenvironments. Clotting, clot contraction, and fibrinolysis stimulated by thrombin or tissue plasminogen activator, respectively, were measured. T2MR signals of clotting samples were compared with images produced by scanning electron microscopy and with standard reference methods for the following parameters: hematocrit, prothrombin time, clot strength, and platelet activity. Application of T2MR methodology revealed conditions under which a unique T2MR signature appeared that corresponded with the formation of polyhedral erythrocytes, the dynamics and morphology of which are dependent on thrombin, fibrinogen, hematocrit, and platelet levels. We also showed that the T2MR platform can be used for precise and accurate measurements of hematocrit (%CV, 4.8%, R(2) = 0.95), clotting time (%CV, 3.5%, R(2) = 0.94), clot strength (R(2) = 0.95), and platelet function (93% agreement with light transmission aggregometry). This proof-of-concept study demonstrates that T2MR has the potential to provide rapid and sensitive identification of patients at risk for thrombosis or bleeding and to identify new biomarkers and therapeutic targets with a single, simple-to-employ analytic approach that may be suitable for routine use in both research and diverse clinical settings.

Trypanosoma brucei, a parasitic protist with a single flagellum, is the causative agent of African sleeping sickness. Propulsion of T. brucei was long believed to be by a drill-like, helical motion. Using millisecond differential interference-contrast microscopy and analyzing image sequences of cultured procyclic-form and bloodstream-form parasites, as well as bloodstream-form cells in infected mouse blood, we find that, instead, motility of T. brucei is by the propagation of kinks, separating left-handed and right-handed helical waves. Kink-driven motility, previously encountered in prokaryotes, permits T. brucei a helical propagation mechanism while avoiding the large viscous drag associated with a net rotation of the broad end of its tapering body. Our study demonstrates that millisecond differential interference-contrast microscopy can be a useful tool for uncovering important short-time features of microorganism locomotion.