Seagrass meadows provide numerous ecosystem services and their rapid global loss may reduce human welfare as well as ecological integrity. In common with the other ‘blue carbon’ habitats (mangroves and tidal marshes) seagrasses are thought to provide coastal defence and encourage sediment stabilisation and surface elevation. A sophisticated understanding of sediment elevation dynamics in mangroves and tidal marshes has been gained by monitoring a wide range of different sites, located in varying hydrogeomorphological conditions over long periods. In contrast, similar evidence for seagrasses is sparse; the present study is a contribution towards filling this gap. Surface elevation change pins were deployed in four locations, Scotland, Kenya, Tanzania and Saudi Arabia, in both seagrass and unvegetated control plots in the low intertidal and shallow subtidal zone. The presence of seagrass had a highly significant, positive impact on surface elevation at all sites. Combined data from the current work and the literature show an average difference of 31 mm per year in elevation rates between vegetated and unvegetated areas, which emphasizes the important contribution of seagrass in facilitating sediment surface elevation and reducing erosion. This paper presents the first multi-site study for sediment surface elevation in seagrasses in different settings and species.

Organisms typically face infection by diverse pathogens, and hosts are thought to have developed specific responses to each type of pathogen they encounter. The advent of transcriptomics now makes it possible to test this hypothesis and compare host gene expression responses to multiple pathogens at a genome-wide scale. Here, we performed a meta-analysis of multiple published and new transcriptomes using a newly developed bioinformatics approach that filters genes based on their expression profile across datasets. Thereby, we identified common and unique molecular responses of a model host species, the honey bee (Apis mellifera), to its major pathogens and parasites: the Microsporidia Nosema apis and Nosema ceranae, RNA viruses, and the ectoparasitic mite Varroa destructor, which transmits viruses. We identified a common suite of genes and conserved molecular pathways that respond to all investigated pathogens, a result that suggests a commonality in response mechanisms to diverse pathogens. We found that genes differentially expressed after infection exhibit a higher evolutionary rate than non-differentially expressed genes. Using our new bioinformatics approach, we unveiled additional pathogen-specific responses of honey bees; we found that apoptosis appeared to be an important response following microsporidian infection, while genes from the immune signalling pathways, Toll and Imd, were differentially expressed after Varroa/virus infection. Finally, we applied our bioinformatics approach and generated a gene co-expression network to identify highly connected (hub) genes that may represent important mediators and regulators of anti-pathogen responses. Our meta-analysis generated a comprehensive overview of the host metabolic and other biological processes that mediate interactions between insects and their pathogens. We identified key host genes and pathways that respond to phylogenetically diverse pathogens, representing an important source for future functional studies as well as offering new routes to identify or generate pathogen resilient honey bee stocks. The statistical and bioinformatics approaches that were developed for this study are broadly applicable to synthesize information across transcriptomic datasets. These approaches will likely have utility in addressing a variety of biological questions.

Honeybees, Apis mellifera, show age-related division of labor in which young adults perform maintenance (“housekeeping”) tasks inside the colony before switching to outside foraging at approximately 23 days old. Disease resistance is an important feature of honeybee biology, but little is known about the interaction of pathogens and age-related division of labor. We tested a hypothesis that older forager bees and younger “house” bees differ in susceptibility to infection. We coupled an infection bioassay with a functional analysis of gene expression in individual bees using a whole genome microarray. Forager bees treated with the entomopathogenic fungus Metarhizium anisopliae s.l. survived for significantly longer than house bees. This was concomitant with substantial differences in gene expression including genes associated with immune function. In house bees, infection was associated with differential expression of 35 candidate immune genes contrasted with differential expression of only two candidate immune genes in forager bees. For control bees (i.e. not treated with M. anisopliae) the development from the house to the forager stage was associated with differential expression of 49 candidate immune genes, including up-regulation of the antimicrobial peptide gene abaecin, plus major components of the Toll pathway, serine proteases, and serpins. We infer that reduced pathogen susceptibility in forager bees was associated with age-related activation of specific immune system pathways. Our findings contrast with the view that the immunocompetence in social insects declines with the onset of foraging as a result of a trade-off in the allocation of resources for foraging. The up-regulation of immune-related genes in young adult bees in response to M. anisopliae infection was an indicator of disease susceptibility; this also challenges previous research in social insects, in which an elevated immune status has been used as a marker of increased disease resistance and fitness without considering the effects of age-related development. Honeybees have a highly developed form of social biology in which tasks are distributed among workers according to their age, with younger bees performing housekeeping tasks (“house bees”) before switching to foraging duties when they grow older. This division of labor is vital to colony function and survival. Pathogens are known to be partly responsible for the current decline in honeybee populations around the world, but we understand little about the responses of different types of worker bee to infection. In this study, we infected house and forager bees with an insect pathogen. We measured bee survival rate and the expression of genes that regulate the immune system. More immune genes were up regulated in house bees than foragers in response to infection, but foragers were more resistant to the pathogen than house bees. We found that development from the house to forager stages resulted in increased expression of genes that regulate the production of antimicrobial proteins. The inference is that parts of the immune system are activated during development, resulting in greater resistance to infectious disease in forager bees. Our study provides new insights into the functioning of the honeybee immune system and its interaction with social organisation.

Aedes aegypti is the vector of a wide range of diseases (e.g. yellow fever, dengue, Chikungunya and Zika) which impact on over half the world’s population. Entomopathogenic fungi such as Metarhizium anisopliae and Beauveria bassiana have been found to be highly efficacious in killing mosquito larvae but only now are the underlying mechanisms for pathogenesis being elucidated. Recently it was shown that conidia of M. anisopliae caused stress induced mortality in Ae. aegypti larvae, a different mode of pathogenicity to that normally seen in terrestrial hosts. Blastospores constitute a different form of inoculum produced by this fungus when cultured in liquid media and although blastospores are generally considered to be more virulent than conidia no evidence has been presented to explain why. In our study, using a range of biochemical, molecular and microscopy methods, the infection process of Metarhizium brunneum (formerly M. anisopliae) ARSEF 4556 blastospores was investigated. It appears that the blastospores, unlike conidia, readily adhere to and penetrate mosquito larval cuticle. The blastospores are readily ingested by the larvae but unlike the conidia are able infect the insect through the gut and rapidly invade the haemocoel. The fact that pathogenicity related genes were upregulated in blastospores exposed to larvae prior to invasion, suggests the fungus was detecting host derived cues. Similarly, immune and defence genes were upregulated in the host prior to infection suggesting mosquitoes were also able to detect pathogen-derived cues. The hydrophilic blastospores produce copious mucilage, which probably facilitates adhesion to the host but do not appear to depend on production of Pr1, a cuticle degrading subtilisin protease, for penetration since protease inhibitors did not significantly alter blastospore virulence. The fact the blastospores have multiple routes of entry (cuticle and gut) may explain why this form of the inoculum killed Ae. aegypti larvae in a relatively short time (12-24hrs), significantly quicker than when larvae were exposed to conidia. This study shows that selecting the appropriate form of inoculum is important for efficacious control of disease vectors such as Ae. aegypti. Mosquitoes transmit a range of diseases which have a profound impact on human health. Aedes aegypti vectors dengue, one of the fastest emerging diseases and, more recently, the Zika virus, which has been linked to thousands of birth defects over the last two years in Brazil. Insect pathogenic fungi such as Metarhizium brunneum are effective in killing mosquito adults and larvae. They exhibit much plasticity, producing aerial conidia on solid substrates and blastospores in liquid media. We not only show that blastospores are more virulent than conidia but present evidence explaining why they are more aggressive. The blastospore mode of pathogenesis differs from that of conidia in several ways. Firstly, blastospores appear to be more dependent on entry using mechanical force than by secretion of cuticle degrading proteases such as Pr1. Blastospores produce copious mucilage which ensures that many spores attach to the cuticle. They are also readily ingested and able to penetrate the gut wall rapidly and colonize the haemocoel. Multiple entry points and gross damage to the cuticle and gut results in rapid larval death. Conidia neither adhere to the cuticle nor germinate in the gut but cause Pr1 stress induced mortality, which takes a slightly longer time. Blastopores, therefore, have greater potential for the control of Ae. aegypti larvae in mosquito control programmes

We use data from the serial passage of co-occluded recombinant Autographa californica nuclear polyhedrosis virus (Ac M NPV) to estimate the viral multiplicity of infection of cells within infected insects. Co-occlusion, the incorporation of wild-type and mutant virus genomes in the same occlusion body, has been proposed as a strategy to deliver genetically modified viruses as insecticides in a way that contains their spread in the environment. It may also serve as a means whereby naturally occurring mutant forms of NPVs can be maintained in a stable polymorphism. Here, a recombinant strain of Ac M NPV was constructed with a deletion of its polyhedrin gene, rendering it incapable of producing occlusion bodies (i.e., occlusion negative). This was co-occluded with wild-type Ac M NPV and used to infect fifth-instar Trichoplusia ni larvae. The fate of both genotypes was monitored over several rounds of insect infection. Levels of the occlusion-negative virus genome declined slowly over successive rounds of infection. We applied these data to a model of NPV population genetics to derive an estimate of 4.3 ± 0.3 viral genomes per occlusion body-producing cell.

Biologging devices are used ubiquitously across vertebrate taxa in studies of movement and behavioural ecology to record data from organisms without the need for direct observation. Despite the dramatic increase in the sophistication of this technology, progress in reducing the impact of these devices to animals is less obvious, notwithstanding the implications for animal welfare. Existing guidelines focus on tag weight (e.g. the ‘5% rule'), ignoring aero/hydrodynamic forces in aerial and aquatic organisms, which can be considerable. Designing tags to minimize such impact for animals moving in fluid environments is not trivial, as the impact depends on the position of the tag on the animal, as well as its shape and dimensions. We demonstrate the capabilities of computational fluid dynamics (CFD) modelling to optimize the design and positioning of biologgers on marine animals, using the grey seal (Halichoerus grypus) as a model species. Specifically, we investigate the effects of (a) tag form, (b) tag size, and (c) tag position and quantify the impact under frontal hydrodynamic forces, as encountered by seals swimming at sea. By comparing a conventional versus a streamlined tag, we show that the former can induce up to 22% larger drag for a swimming seal; to match the drag of the streamlined tag, the conventional tag would have to be reduced in size by 50%. For the conventional tag, the drag induced can differ by up to 11% depending on the position along the seal's body, whereas for the streamlined tag this difference amounts to only 5%. We conclude by showing how the CFD simulation approach can be used to optimize tag design to reduce drag for aerial and aquatic species, including issues such as the impact of lateral currents (unexplored until now). We also provide a step‐by‐step guide to facilitate the implementation of CFD in biologging tag design.