Hohen Neuendorf, Germany
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News Article | March 2, 2017
Site: www.eurekalert.org

A core set of genes involved in the responses of honey bees to multiple diseases caused by viruses and parasites has been identified by an international team of researchers. The findings provide a better-defined starting point for future studies of honey-bee health, and may help scientists and beekeepers breed honey bees that are more resilient to stress. "In the past decade, honey-bee populations have experienced severe and persistent losses across the Northern Hemisphere, mainly due to the effects of pathogens, such as fungi and viruses," said Vincent Doublet, postdoctoral research fellow, University of Exeter. "The genes that we identified offer new possibilities for the generation of honey-bee stocks that are resistant to these pathogens." According to the researchers, recent advances in DNA sequencing have prompted numerous investigations of the genes involved in honey-bee responses to pathogens. Yet, until now, this vast quantity of data has been too cumbersome and idiosyncratic to reveal overarching patterns in honey-bee immunity. "While many studies have used genomic approaches to understand how bees respond to viruses and parasites, it has been difficult to compare across these studies to find the core genes and pathways that help the bee fight off stressors," said Distinguished Professor of Entomology Christina Grozinger, Penn State. "Our team created a new bioinformatics tool that has enabled us to integrate information from 19 different genomic datasets to identify the key genes involved in honey bees' response to diseases." Specifically, the team of 28 researchers, representing eight countries, created a new statistical technique, called directed rank-product analysis. The technique allowed them to identify the genes that were expressed similarly across the 19 datasets, rather than just the genes that were expressed more than others within a dataset. The scientists found that these similarly expressed genes included those that encode proteins responsible for the response to tissue damage by pathogens, and those that encode enzymes involved in the metabolism of carbohydrates from food, among many others. A decrease in carbohydrate metabolism, they suggested, may illustrate the cost of the infection on the organism. The researchers report their findings in today's (Mar. 2) issue of BMC Genomics. "Honey bees were thought to respond to different disease organisms in entirely different ways, but we have learned that they mostly rely on a core set of genes that they turn on or off in response to any major pathogenic challenge," said Robert Paxton, professor of zoology, German Centre for Integrative Biodiversity Research. "We can now explore the physiological mechanisms by which pathogens overcome their honey-bee hosts, and how honey bees can fight back against those pathogens." The implications of the findings are not limited to honey bees. The team found that the core genes are part of conserved pathways -- meaning they have been maintained throughout the course of evolution among insects and therefore are shared by other insects. According to Doublet, this means that the genes provide important knowledge for understanding pathogen interactions with other insects, such as bumble bees, and for using pathogens to control insect pests, such as aphids and certain moths. "This analysis provides unprecedented insight into the mechanisms that underpin the interactions between insects and their pathogens," said Doublet. "With this analysis, we generated a list of genes that will likely be an important source for future functional studies, for breeding more resilient honey-bee stocks and for controlling emerging bee diseases." This research was supported by iDiv, the German Center for Integrative Biodiversity Research, located in Leipzig, Germany. Other authors on the paper include Yvonne Poeschl, German Centre for Integrative Biodiversity Research; Andreas Gogol-Döring, Technische Hochschule Mittelhessen; Cédric Alaux, INRA; Desiderato Annoscia, Università degli Studi di Udine; Christian Aurori, University of Agricultural Sciences and Veterinary Medicine of Cluj-Napoca; Seth Barribeau, University of Liverpool; Oscar Bedoya-Reina, University of Edinburgh; Mark Brown, Royal Holloway University of London; James Bull, Swansea University; Michelle Flenniken, Montana State University; David Galbraith, Penn State; Elke Genersch, Institute for Bee Research of Hohen Neuendorf; Sebastian Gisder, Institute for Bee Research of Hohen Neuendorf; Ivo Grosse, Martin Luther University Halle-Wittenberg; Holly Holt, University of Minnesota; Dan Hultmark, Umeå University; H. Michael G. Lattorff, International Centre of Insect Physiology and Ecology; Yves Le Conte, INRA; Fabio Manfredini, Royal Holloway University of London; Dino McMahon, Freie Universität Berlin; Robin Moritz, Martin Luther University Halle-Wittenberg; Francesco Nazzi, Università degli Studi di Udine; Elina Niño, University of California, Davis; Katja Nowick, University of Leipzig; and Ronald van Rij, Radboud University.

Garcia-Gonzalez E.,Institute for Bee Research | Garcia-Gonzalez E.,Humboldt University of Berlin | Genersch E.,Institute for Bee Research
Environmental Microbiology | Year: 2013

Summary: Paenibacillus larvae, the aetiological agent of American foulbrood (AFB) of honey bees, causes a fatal intestinal infection in larvae and invades the haemocoel by breaching the midgut. The peritrophic matrix lining the midgut epithelium in insects constitutes an effective barrier against abrasive food particles, xenobiotics, toxins and pathogens. Pathogens like P.larvae entering the host through the gut first need to overcome this barrier. To better understand AFB pathogenesis, we analysed the fate of the peritrophic matrix in honey bee larvae during P.larvae infection. Using histochemical techniques, we first established that chitin is a major component of the honey bee larval peritrophic matrix. Rearing larvae on a diet containing a fluorochrome blocking formation of the peritrophic matrix or a bacterial endochitinase revealed that a fully formed peritrophic matrix is essential for larval survival. Larvae infected by P.larvae showed total degradation of the peritrophic matrix enabling the bacteria to directly attack the epithelial cells. Carbon source utilization tests confirmed that P.larvae is able to metabolize colloidal chitin. We propose that P.larvae degrades the peritrophic matrix to allow direct access of the bacteria or of bacterial toxins to the epithelium to prepare the breakthrough of the epithelial layer. © 2013 Society for Applied Microbiology and John Wiley & Sons Ltd.

Genersch E.,Institute for Bee Research
Journal of Invertebrate Pathology | Year: 2010

After more than a century of American Foulbrood (AFB) research, this fatal brood infection is still among the most deleterious bee diseases. Its etiological agent is the Gram-positive, spore-forming bacterium Paenibacillus larvae. Huge progress has been made, especially in the last 20 years, in the understanding of the disease and of the underlying host-pathogen interactions. This review will place these recent developments in the study of American Foulbrood and of P. larvae into the general context of AFB research. © 2009 Elsevier Inc. All rights reserved.

de Miranda J.R.,Swedish University of Agricultural Sciences | Genersch E.,Institute for Bee Research
Journal of Invertebrate Pathology | Year: 2010

Deformed wing virus (DWV; Iflaviridae) is one of many viruses infecting honeybees and one of the most heavily investigated due to its close association with honeybee colony collapse induced by Varroa destructor. In the absence of V. destructor DWV infection does not result in visible symptoms or any apparent negative impact on host fitness. However, for reasons that are still not fully understood, the transmission of DWV by V. destructor to the developing pupae causes clinical symptoms, including pupal death and adult bees emerging with deformed wings, a bloated, shortened abdomen and discolouration. These bees are not viable and die soon after emergence. In this review we will summarize the historical and recent data on DWV and its relatives, covering the genetics, pathobiology, and transmission of this important viral honeybee pathogen, and discuss these within the wider theoretical concepts relating to the genetic variability and population structure of RNA viruses, the evolution of virulence and the development of disease symptoms. © 2009 Elsevier Inc. All rights reserved.

Gisder S.,Institute for Bee Research | Genersch E.,Institute for Bee Research
Journal of Invertebrate Pathology | Year: 2013

Nosema apis and Nosema ceranae are two microsporidian pathogens of the European honey bee, Apis mellifera. There is evidence that N. ceranae is more virulent than N. apis subject to environmental factors like climate. This makes N. ceranae one of the suspects in the increasing colony losses recently observed in many regions of the world. Correct differentiation between N. apis and N. ceranae is important and best accomplished by molecular methods. So far only protocols based on species-specific sequence differences in the 16S rRNA gene are available. However, recent studies indicated that these methods may lead to confusing results due to polymorphisms in and recombination between the multi-copy 16S rRNA genes. To solve this problem and to provide a reliable molecular tool for the differentiation between the two bee pathogenic microsporidia we here present and evaluate a duplex-PCR protocol based on species-specific sequence differences in the highly conserved gene coding for the DNA-dependent RNA polymerase II largest subunit. A total of 102 honey bee samples were analyzed by the novel PCR protocol and the results were compared with the results of the originally published PCR-RFLP analysis and two recently published differentiation protocols, based on 16S rRNA sequence differences. Although the novel PCR protocol proved to be as reliable as the 16S rRNA gene based PCR-RFLP it was superior to simple 16S rRNA based PCR protocols which tended to overestimate the rate of N. ceranae infections. Therefore, we propose that species-specific sequence differences of highly conserved protein coding genes should become the preferred molecular tool for differentiation of Nosema spp. © 2013 Elsevier Inc.

Lichtenberg-Kraag B.,Institute for Bee Research
Journal of Apicultural Research | Year: 2014

Analysis of the honey enzymes diastase and invertase is one important parameter in honey quality control. Limits for enzyme activity are given by food legislation or directives of national brands, because enzyme activity is one of the measures of adequate conversion of nectar to honey during the ripening process. In addition, certain activity levels of invertase or diastase activity can also act as indicators for heat damage of honey samples. Depending on the botanical origin, enormous differences in enzyme activity can be observed, even though the enzymes are mostly added by the bees. We therefore collected nectar and honey samples during the ripening process of honey and investigated enzyme activity depending on the floral source. Based on the analysis of nectar samples, we could demonstrate that floral source and environmental conditions affect the total sugars and sucrose concentration. We therefore hypothesized that the composition of the nectar, especially the amount of sucrose, may interact with the activity of invertase. We found that correlation between sucrose concentration and invertase activity is highly significant during the ripening process of honey (p < 0.0001) confirming an interaction between these two parameters. This effect was further substantiated by a sugar feeding experiment with defined sucrose concentrations. Possibly a high turn-over at high sucrose concentrations may lead to enzyme exhaustion for invertase.

McMenamin A.J.,Pennsylvania State University | Genersch E.,Institute for Bee Research
Current Opinion in Insect Science | Year: 2015

Recent large-scale colony losses among managed Western honey bees (Apis mellifera) have alarmed researchers and apiculturists alike. Here, the existing correlative evidence provided by monitoring studies is reviewed which (i) identified members of the deformed wing virus and acute bee paralysis virus clades as lethal pathogens for entire colonies, and (ii) identified novel viruses whose impact on honey bee health remains elusive. Also discussed in this review is related evidence obtained via controlled experimental infection assays and RNAi approaches underscoring the damage inflicted by some of these viruses on individuals and colonies. The relevance of the ectoparasitic mite Varroa destructor acting as mechanical and biological virus vector for the enhanced virulence of certain viruses or mite selected virus strains is carefully considered. © 2015 Elsevier Inc.

Funfhaus A.,Institute for Bee Research | Poppinga L.,Institute for Bee Research | Genersch E.,Institute for Bee Research
Environmental Microbiology | Year: 2013

Summary: Paenibacillus larvae is a Gram-positive bacterial pathogen causing the epizootic American foulbrood in honey bee larvae. Four so-called enterobacterial repetitive intergenic consensus (ERIC) genotypes of P.larvae exist with P.larvae genotypes ERIC I and ERIC II being responsible for disease outbreaks all over the world. Very few molecular data on the pathogen, on pathogenesis or on virulence factors exist. We now identified two genomic loci in P.larvaeERIC I coding for two binary AB toxins, Plx1 and Plx2. In silico analyses revealed that Plx1 is the third member of an enigmatic family of AB toxins so far only comprising MTX1 of Lysinibacillus sphaericus and pierisin-like toxins expressed by several butterflies. Plx2 is also remarkable because the A-domain is highly similar to C3 exoenzymes, which normally are single domain proteins, while the B-domain is homologous to B-domains of C2-toxins. We constructed P.larvae mutants lacking expression of Plx1, Plx2 or both toxins and demonstrated that these toxins are important virulence factors for P.larvaeERIC I. © 2013 Society for Applied Microbiology and John Wiley & Sons Ltd.

Poppinga L.,Institute for Bee Research | Genersch E.,Institute for Bee Research
Current Opinion in Insect Science | Year: 2015

American Foulbrood caused by Paenibacillus larvae is one of the unsolved health problems honey bee colonies are suffering from. In the recent past, considerable progress has been achieved in understanding molecular details of P. larvae infections of honey bee larvae. This was facilitated by the development of molecular tools for manipulating P. larvae and by the availability of complete genome sequences of different P. larvae genotypes. We here report on several peptides and proteins that have recently been identified, biochemically analyzed, and proposed to act as virulence factors of P. larvae. For some of them, experimental proof for their role as virulence factor has been provided allowing presenting a preliminary model for the molecular pathogenesis of American Foulbrood. © 2015 Elsevier Inc. All rights reserved.

Funfhaus A.,Institute for Bee Research | Genersch E.,Institute for Bee Research
Environmental Microbiology Reports | Year: 2012

Honey bee pathology has attracted much interest recently due to the problems with honey bee declines in many regions of the world. American Foulbrood (AFB) caused by Paenibacillus larvae is the most devastating bacterial brood disease of the Western honey bee (Apis mellifera) causing considerable economic losses to beekeepers worldwide. AFB outbreaks are mainly caused by two differentially virulent genotypes of P.larvae, P.larvae ERIC I and ERIC II. To better understand AFB pathogenesis and to complement already existing data from the genetic level we aimed at obtaining expression data from the protein level. We successfully developed a protocol for two-dimensional proteome analysis of P.larvae with subsequent mass-spectrometry based protein sequencing. Based on the obtained master protein maps of P.larvae genotypes ERIC I and II we identified the dominantly expressed cytosolic proteins of both genotypes, some of them presumably linked to pathogenesis and virulence. Comparing the master maps of both genotypes revealed differentially expressed proteins, i.e. a putative S-layer protein which is expressed by P.larvae ERIC II but absent from the proteome of P.larvae ERIC I. The implications of our findings for pathogenesis of AFB and virulence of P.larvae will be discussed. © 2012 Society for Applied Microbiology and Blackwell Publishing Ltd.

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