Variation In Disease Resistance Research Articles

Genetic variation in disease resistance in Drosophila spp. is mitigated in Drosophila sechellia by specialization to a toxic host

We found that Drosophila species vary in their susceptibility to the broad-spectrum entomopathogen, Metarhizium anisopliae (strain Ma549). Generalist species were generally more resistant than dietary specialists, with the cactophilic Drosophila buzzatii and Drosophila sechellia, a specialist of the Morinda citrifolia (Morinda) fruit, being most susceptible. Morinda fruit is reported to be toxic to most herbivores because it contains Octanoic Acid (OA). We confirmed that OA is toxic to Drosophila spp., other than D. sechellia, and we also found that OA is highly toxic to entomopathogenic fungi including Ma549 and Beauveria bassiana. Drosophilasechellia fed a diet containing OA, even at levels much less than found in Morinda fruit, had greatly reduced susceptibility to Ma549. This suggests that specializing to Morinda may have provided an enemy-free space, reducing adaptive prioritization on a strong immune response. Our results demonstrate that M. anisopliae and Drosophila species with divergent lifestyles provide a versatile model system for understanding the mechanisms of host–pathogen interactions at different scales and in environmental context.

Selection for disease resistance in Oncorhynchus mykissincreases the myeloid to lymphoid balance and is affected by rapamycin as measured by flow cytometry and scRNAseq.

Abstract Heritable variation in disease resistance has been described in many species, but the effects of selection on innate immunity are unclear. Here, we compare the cellular response of two lines of rainbow trout that differ in survival due to five generations of selection for resistance to Flavobacterium psychrophilum(Fp), an important fish pathogen. We examined bacterial load, plasma biomarkers, whole blood cellular composition, and blood chemistry at days 1 and 5 after bacterial or PBS injection. We also examined the effect of 0.8 mg/kg rapamycin pretreatment, which results in immunosuppression and a ~100-fold reduction in the challenge LD 50. On day 1, bacterial load did not differ between genetic lines and treatment, but by day 5, the R-line exhibited no increase in Fpload, while rapamycin increased R- and S-line loads 33- and 506-fold, respectively. Biomarkers: cathelicidin 2 and C1q-LP3 significantly differed between genetic lines and by time, corresponding to Fpload. Analysis of whole blood by flow cytometry identified a response to infection and an ~8 percentage point higher frequency of myeloid-gated cells in R-line fish that was consistent in both naïve and challenged animals. S-line fish exhibited a higher percentage of IgM +B cells. Single-cell RNAseq was conducted on day 1 purified blood and identified 23 cell clusters including multiple B cell, neutrophil and macrophage subpopulations. In naïve animals, S-line fish harbored a cxcr4and mychexpressing B cell subpopulation absent in R-line fish. Rapamycin pretreatment caused profound loss of multiple B cell subpopulations in R- and S-line fish. In summary, selection of rainbow trout for resistance to Fpis correlated with a cellular shift in peripheral blood and is mTOR dependent. US Department of Agriculture, Agricultural Research Service; Project number 1930-32000-007

Specific resistance prevents the evolution of general resistance and facilitates disease emergence.

Host-shifts, where pathogens jump from an ancestral host to a novel host, can be facilitated or impeded by standing variation in disease resistance, but only if resistance provides broad-spectrum general resistance against multiple pathogen species. Host resistance comes in many forms and includes both general resistance, as well as specific resistance, which may only be effective against a single pathogen species or even genotype. However, most evolutionary models consider only one of these forms of resistance, and we have less understanding of how these two forms of resistance evolve in tandem. Here, we develop a model that allows for the joint evolution of specific and general resistance and asks if the evolution of specific resistance drives a decrease in the evolution of general resistance. We also explore how these evolutionary outcomes affect the risk of foreign pathogen invasion and persistence. We show that in the presence of a single endemic pathogen, the two forms of resistance are strongly exclusionary. Critically, we find that specific resistance polymorphisms can prevent the evolution of general resistance, facilitating the invasion of foreign pathogens. We also show that specific resistance polymorphisms are a necessary condition for the successful establishment of foreign pathogens following invasion, as they prevent the exclusion of the foreign pathogen by the more transmissible endemic pathogen. Our results demonstrate the importance of considering the joint evolution of multiple forms of resistance when evaluating a population's susceptibility to foreign pathogens.

Identification of Pathogens and Evaluation of Resistance and Genetic Diversity of Maize Inbred Lines to Stalk Rot in Heilongjiang Province, China.

Maize stalk rot, caused by multiple pathogens, is a serious soilborne disease worldwide. Composition of pathogens causing maize stalk rot and resistance of maize inbred lines in Heilongjiang Province, China, are not well understood. In this study, 138 fungal isolates were collected from different maize-producing areas in Heilongjiang Province, which were identified as Fusarium graminearum (23.2%), F. subglutinans (18.9%), F. cerealis (18.9%), Bipolaris zeicola (13.0%), F. brachygibbosum (13.0%), F. temperatum (7.2%), and F. proliferatum (5.8%). Among them, F. graminearum (>20%) was the predominant species among the isolates causing maize stalk rot. B. zeicola had not previously been reported causing maize stalk rot in China. Resistance of 67 maize inbred lines to maize stalk rot was assessed, and 24 lines (35.8% of them) were highly resistant or resistant, indicating that approximately 65% of these lines were susceptible to maize stalk rot. Maize inbred lines were analyzed using simple sequence repeat markers and divided into five genetic groups with 12 pairs of primers. Additionally, analysis of molecular variance indicated that 44.2% of the genetic variation in disease resistance was distributed among populations. This study provides insight into the genetic diversity of inbred maize and may contribute useful information for breeding stalk rot disease-resistant hybrids, and facilitates development of effective strategies for managing this destructive disease complex.

AIG2A and AIG2B limit the activation of salicylic acid-regulated defenses by tryptophan-derived secondary metabolism in Arabidopsis.

Chemical defense systems involving tryptophan-derived secondary metabolites (TDSMs) and salicylic acid (SA) are induced by general nonself signals and pathogen signals, respectively, in Arabidopsis thaliana. Whether and how these chemical defense systems are connected and balanced is largely unknown. In this study, we identified the AVRRPT2-INDUCED GENE2A (AIG2A) and AIG2B genes as gatekeepers that prevent activation of SA defense systems by TDSMs. These genes also were identified as important contributors to natural variation in disease resistance among A. thaliana natural accessions. The loss of AIG2A and AIG2B function leads to upregulation of both SA and TDSM defense systems. Suppressor screens and genetic analysis revealed that a functional TDSM system is required for the upregulation of the SA pathway in the absence of AIG2A and AIG2B, but not vice versa. Furthermore, the AIG2A and AIG2B genes are co-induced with TDSM biosynthesis genes by general pathogen elicitors and nonself signals, thereby functioning as a feedback control of the TDSM defense system, as well as limiting activation of the SA defense system by TDSMs. Thus, this study uncovers an AIG2A- and AIG2B-mediated mechanism that fine-tunes and balances SA and TDSM chemical defense systems in response to nonpathogenic and pathogenic microbes.

Benefit of Introgression Depends on Level of Genetic Trait Variation in Cereal Breeding Programmes.

We investigated the benefit from introgression of external lines into a cereal breeding programme and strategies that accelerated introgression of the favourable alleles while minimising linkage drag using stochastic computer simulation. We simulated genomic selection for disease resistance and grain yield in two environments with a high level of genotype-by-environment interaction (G × E) for the latter trait, using genomic data of a historical barley breeding programme as the base generation. Two populations (existing and external) were created from this base population with different allele frequencies for few (N = 10) major and many (N ~ 990) minor simulated disease quantitative trait loci (QTL). The major disease QTL only existed in the external population and lines from the external population were introgressed into the existing population which had minor disease QTL with low, medium and high allele frequencies. The study revealed that the benefit of introgression depended on the level of genetic variation for the target trait in the existing cereal breeding programme. Introgression of external resources into the existing population was beneficial only when the existing population lacked variation in disease resistance or when minor disease QTL were already at medium or high frequency. When minor disease QTL were at low frequencies, no extra genetic gain was achieved from introgression. More benefit in the disease trait was obtained from the introgression if the major disease QTL had larger effect sizes, more selection emphasis was applied on disease resistance, or more external lines were introgressed. While our strategies to increase introgression of major disease QTL were generally successful, most were not able to completely avoid negative impacts on selection for grain yield with the only exception being when major introgression QTL effects were very large. Breeding programmes are advised to carefully consider the level of genetic variation in a trait available in their breeding programme before deciding to introgress germplasms.

Bacterial Lipopolysaccharide Activates Toll-Like Receptor 2 and Toll-Like Receptor 4 Gene Expression in PBMC of Vechur Cattle

Vechur cattle, an indigenous breed of Kerala and it is the smallest cattle breed in the world. They are highly disease resistant. The occurrence of mastitis is very Rare in this breed as compared to crossbred cattle. Rearing of these Vechur breed is more cost effective as they require less feed. Therefore, characterisation of factors involved in the immune system of these breeds might provide an insight into the mechanisms involved in the variation in disease resistance. Toll-like receptors (TLRs) are part of the innate immunity, can recognize the particular pathogens through Pathogen Associated Molecular pattern s (PAMPs) and play important roles in host defense. TLR2 and TLR4 important TLR mediate the responsiveness to bacterial lipopolysaccharide (LPS). Since Vechur cattle are less susceptible to mastitis, in vitro expression assay of TLRs were accessed by challenging the Peripheral Blood Mononuclear Cells (PBMC) with bacterial LPS. Treatment of PBMC with LPS, significantly increased TLR2 and TLR4 genes expression (p≤0.01) in Vechur cattle breed when compared with that of control and crossbred cattle. Among the two TLRs studied, the relative expression of mRNA in Vechur cattle was relatively higher for TLR2 (6.90) than TLR4 (4.24). The higher expression of TLR 2 and TLR 4might contribute maximum innate immune response against the mastitis bacteria in Vechur cattle.

Intraspecific host variation plays a key role in virus community assembly

Infection by multiple pathogens of the same host is ubiquitous in both natural and managed habitats. While intraspecific variation in disease resistance is known to affect pathogen occurrence, how differences among host genotypes affect the assembly of pathogen communities remains untested. In our experiment using cloned replicates of naive Plantago lanceolata plants as sentinels during a seasonal virus epidemic, we find non-random co-occurrence patterns of five focal viruses. Using joint species distribution modelling, we attribute the non-random virus occurrence patterns primarily to differences among host genotypes and local population context. Our results show that intraspecific variation among host genotypes may play a large, previously unquantified role in pathogen community structure.

In vitro phagocytosis of opsonized latex beads by HD11 cells as a method to assess the general opsonization potential of chicken serum

ABSTRACTOpsonins, an important arm of the innate immune system, are various soluble proteins, which play a critical role in destruction of invading pathogens directly or via engulfment of pathogens through the intermediate of phagocytosis. The diversity of opsonin profiles is under genetic influence and may be associated with variation in disease resistance. The aim of this study was to set up an assay to determine serum opsonophagocytic potential (OPp) for chicken sera by flow cytometry and to evaluate the assay using samples from different chicken lines. Two chicken lines selected for high and low concentrations of mannose-binding lectin, a known opsonin, in serum were used to establish the method. Furthermore, the presumed “robust” Hellevad chickens and two other commercial chicken lines (Hisex and Bovans) were tested to evaluate OPp as a parameter reflecting general immune competence. The results showed that Hellevad and Bovans chickens had higher OPp than Hisex chickens. There were no correlations between concentrations of total IgY or mannose-binding lectin and OPp. However, a strong positive correlation was observed between vaccine-induced infectious bronchitis virus titres and OPp. Moreover, inverse relationships were observed between concentrations of total serum IgM as well as natural antibody levels, and OPp. In conclusion, in vitro opsonophagocytosis assessment and determination of OPp may be of relevance when addressing general innate immunocompetence.RESEARCH HIGHLIGHTSA flow cytometry method was developed to assess poultry serum opsonophagocytosis potential.This method is based on serum-opsonin-coated polystyrene beads and HD11 cell phagocytosis.Serum samples from different commercial chicken lines were compared.Opsonophagocytic potential may be included in assay panels for general immune competence of poultry.

NLR Mutations Suppressing Immune Hybrid Incompatibility and Their Effects on Disease Resistance.

Genetic divergence between populations can lead to reproductive isolation. Hybrid incompatibilities (HI) represent intermediate points along a continuum toward speciation. In plants, genetic variation in disease resistance (R) genes underlies several cases of HI. The progeny of a cross between Arabidopsis (Arabidopsis thaliana) accessions Landsberg erecta (Ler, Poland) and Kashmir2 (Kas2, central Asia) exhibits immune-related HI. This incompatibility is due to a genetic interaction between a cluster of eight TNL (TOLL/INTERLEUKIN1 RECEPTOR-NUCLEOTIDE BINDING-LEU RICH REPEAT) RPP1 (RECOGNITION OF PERONOSPORA PARASITICA1)-like genes (R1-R8) from Ler and central Asian alleles of a Strubbelig-family receptor-like kinase (SRF3) from Kas2. In characterizing mutants altered in Ler/Kas2 HI, we mapped multiple mutations to the RPP1-like Ler locus. Analysis of these suppressor of Ler/Kas2 incompatibility (sulki) mutants reveals complex, additive and epistatic interactions underlying RPP1-like Ler locus activity. The effects of these mutations were measured on basal defense, global gene expression, primary metabolism, and disease resistance to a local Hyaloperonospora arabidopsidis isolate (Hpa Gw) collected from Gorzów (Gw), where the Landsberg accession originated. Gene expression sectors and metabolic hallmarks identified for HI are both dependent and independent of RPP1-like Ler members. We establish that mutations suppressing immune-related Ler/Kas2 HI do not compromise resistance to Hpa Gw. QTL mapping analysis of Hpa Gw resistance point to RPP7 as the causal locus. This work provides insight into the complex genetic architecture of the RPP1-like Ler locus and immune-related HI in Arabidopsis and into the contributions of RPP1-like genes to HI and defense.

QNCLB7.02, a novel QTL for resistance to northern corn leaf blight in maize

Northern corn leaf blight (NCLB), which is caused by the hemibiotrophic fungal pathogen Setosphaeria turcica, is a devastating foliar disease that results in considerable maize yield losses. In the present study, quantitative trait locus (QTL) analysis was conducted across two environments using an ultra-high-density bin map constructed using recombinant inbred lines (RILs) derived from a cross between Ye478 and Qi319. A total of 11 QTLs, located on chromosomes 1, 4, 5, 6, 7, 8, 9, and 10, were detected that confer resistance to physiological race 0 of NCLB. Each QTL could explain 3.53–15.29% of the total phenotypic variation in disease resistance after artificial inoculation in two environments. Among these QTL, qNCLB7.02, which is located on chromosome 7, had the largest effect, accounting for 10.11 and 15.29% of the phenotypic variation in resistance in two field trials and BLUP. The common confidence interval (CI) for qNCLB7.02 was 1.4 Mb, according to the B73 RefGen_v3 sequence. The resistance effect of qNCLB7.02 was validated in 2016 by using chromosome segment substitution lines (CSSLs) derived from Qi319 as the donor in the genetic background of Ye478. The type 6 CSSL, which harbors introgressed qNCLB7.02, was found to be significantly associated with resistance to NCLB by linked marker bnlg1808 and exhibited greater resistance than the other CSSLs that did not carry this QTL (P = 0.0008). The combination of linkage mapping in RILs and validation in CSSLs is a powerful approach for the dissection of QTL for disease resistance in maize.

Influence of immunogenetics, sex and body condition on the cutaneous microbial communities of two giant salamanders.

The complex association between hosts and microbial symbionts requires the implementation of multiple approaches to evaluate variation in host physiology. Within amphibians, heterogeneity in immunogenetic traits and cutaneous microbiota is associated with variation in disease resistance. Ozark (Cryptobranchus alleganiensis bishopi) and eastern hellbenders (C.a.alleganiensis) provide a model system to assess variation in host traits and microbial communities. Ozark hellbenders have experienced declines throughout their range, are federally endangered and experience wound retardation that is absent in the eastern subspecies. Previous microbial investigations indicate differentiation in the composition of the skin microbiota of both hellbender subspecies, but it is not clear whether these patterns are concurrent with diversity in the major histocompatibility complex (MHC) genes. We characterized the MHC IIB and the skin microbiota of hellbenders in Missouri, where both subspecies co-occur though not sympatric. We compared the microbiota composition and MHC diversity between both subspecies and investigated whether individual-level MHC diversity, sex and body condition were associated with microbiota composition. Overall, MHC IIB diversity was lower in Ozark hellbenders compared to the eastern subspecies. Multivariate statistical comparisons identified microbiota differentiation between Ozark and eastern hellbenders. MHC IIB allele presence/absence, allele divergence, body composition and sex defined grouping of hellbender microbiotas within populations. Differentiation of the cutaneous microbiotas and MHC IIB genes between eastern and Ozark hellbenders suggests that differences exist in immunity between the two subspecies. This study demonstrates how simultaneous assessments of host genetic traits and microbiotas can inform patterns of microbial community structure in natural systems.

Resistance of Prairie Junegrass and Tufted Hairgrass Germplasm to Diseases Common in Temperate Low-Input Turfgrass Systems

Prairie junegrass and tufted hairgrass are two turfgrass species that are native to the United States and require less water, fertilizer, and pesticide compared with more commonly used turfgrass species such as Kentucky bluegrass. However, little is known about the resistance of these low-input turfgrasses to common turfgrass diseases. The primary objective of this research was to identify disease-resistant germplasm of both prairie junegrass and tufted hairgrass that can be used in future low-input turfgrass breeding efforts. A total of 41 populations of tufted hairgrass and 23 populations of prairie junegrass were evaluated for resistance to Microdochium patch, dollar spot, and rust development in a controlled environment. Genetic variation in disease resistance was clearly present in the unimproved germplasm of both prairie junegrass and tufted hairgrass, providing important direction for future breeding efforts that will allow wider implementation of low-input turfgrass species.

Intraspecific differences in molecular stress responses and coral pathobiome contribute to mortality under bacterial challenge in Acropora millepora

Disease causes significant coral mortality worldwide; however, factors responsible for intraspecific variation in disease resistance remain unclear. We exposed fragments of eight Acropora millepora colonies (genotypes) to putatively pathogenic bacteria (Vibrio spp.). Genotypes varied from zero to >90% mortality, with bacterial challenge increasing average mortality rates 4–6 fold and shifting the microbiome in favor of stress-associated taxa. Constitutive immunity and subsequent immune and transcriptomic responses to the challenge were more prominent in high-mortality individuals, whereas low-mortality corals remained largely unaffected and maintained expression signatures of a healthier condition (i.e., did not launch a large stress response). Our results suggest that lesions appeared due to changes in the coral pathobiome (multiple bacterial species associated with disease) and general health deterioration after the biotic disturbance, rather than the direct activity of any specific pathogen. If diseases in nature arise because of weaknesses in holobiont physiology, instead of the virulence of any single etiological agent, environmental stressors compromising coral condition might play a larger role in disease outbreaks than is currently thought. To facilitate the diagnosis of compromised individuals, we developed and independently cross-validated a biomarker assay to predict mortality based on genes whose expression in asymptomatic individuals coincides with mortality rates.

Studying the Genetics of Resistance to CyHV-3 Disease Using Introgression from Feral to Cultured Common Carp Strains

Sustainability and further development of aquaculture production are constantly challenged by outbreaks of fish diseases, which are difficult to prevent or control. Developing fish strains that are genetically resistant to a disease is a cost-effective and a sustainable solution to address this challenge. To do so, heritable genetic variation in disease resistance should be identified and combined together with other desirable production traits. Aquaculture of common carp has suffered substantial losses from the infectious disease caused by the cyprinid herpes virus type 3 (CyHV-3) virus and the global spread of outbreaks indicates that many cultured strains are susceptible. In this research, CyHV-3 resistance from the feral strain “Amur Sassan” was successfully introgressed into two susceptible cultured strains up to the first backcross (BC1) generation. Variation in resistance of families from F1 and BC1 generations was significantly greater compared to that among families of any of the susceptible parental lines, a good starting point for a family selection program. Considerable additive genetic variation was found for CyHV-3 resistance. This phenotype was transferable between generations with contributions to resistance from both the resistant feral and the susceptible cultured strains. Reduced scale coverage (mirror phenotype) is desirable and common in cultured strains, but so far, cultured mirror carp strains were found to be susceptible. Here, using BC1 families ranging from susceptible to resistant, no differences in resistance levels between fully scaled and mirror full-sib groups were found, indicating that CyHV-3 resistance was successfully combined with the desirable mirror phenotype. In addition, the CyHV-3 viral load in tissues throughout the infection of susceptible and resistant fish was followed. Although resistant fish get infected, viral loads in tissues of these fish are significantly lesser than in those of susceptible fish, allowing them to survive the disease. Taken together, in this study we have laid the foundation for breeding CyHV-3-resistant strains and started to address the mechanisms underlying the phenotypic differences in resistance to this disease.

Genetic resistance to infections in sheep

This paper considers genetic resistance to infectious disease in sheep, with appropriate comparison with goats, and explores how such variation may be used to assist in disease control. Many studies have attempted to quantify the extent to which host animals differ genetically in their resistance to infection or in the disease side-effects of infection, using either recorded animal pedigrees or information from genetic markers to quantify the genetic variation. Across all livestock species, whenever studies are sufficiently well powered, then genetic variation in disease resistance is usually seen and such evidence is presented here for three infections or diseases of importance to sheep, namely mastitis, foot rot and scrapie. A further class of diseases of importance in most small ruminant production systems, gastrointestinal nematode infections, is outside the scope of this review. Existence of genetic variation implies the opportunity, at least in principle, to select animals for increased resistance, with such selection ideally used as part of an integrated control strategy. For each of the diseases under consideration, evidence for genetic variation is presented, the role of selection as an aid to disease control is outlined and possible side effects of selection in terms of effects in performance, effects on resistance to other diseases and potential parasite/pathogen coevolution risks are considered. In all cases, the conclusion is drawn that selection should work and it should be beneficial, with the main challenge being to define cost effective selection protocols that are attractive to sheep farmers.

Estimating heritability of disease resistance and factors that contribute to long-term survival in butternut (Juglans cinerea L.)

For most wild species affected by exotic pests or pathogens, the relative importance of heritable genetic differences in determining apparent variation in disease resistance is unknown. This is true in particular for butternut, a North American hardwood affected by butternut canker disease and undergoing demographic contraction. Little is known about site effects on butternut decline, in part because long-term monitoring data are lacking. We collected detailed disease phenotypes and multilocus microsatellite genotypes for all surviving individuals in a large natural population of butternut in 2003 (n = 302) and 2012 (n = 113). Two analytical methods, correlations between pairwise phenotypic similarity and pairwise relatedness, and estimation of among-family variance, both indicated weak heritability of disease-related traits and no heritability for overall tree health in the population. Additionally, an analysis of spatial data collected in 2001 (n = 341) and 2012 (n = 113) demonstrated that drier, upland sites contribute to increased likelihood of survival. We conclude that genetic differences among wild butternut individuals contributed little to observed variance in survival over 10 years but fine-scale site differences were useful predictors of butternut mortality.

Whole-body transcriptome of selectively bred, resistant-, control-, and susceptible-line rainbow trout following experimental challenge with Flavobacterium psychrophilum.

Genetic improvement for enhanced disease resistance in fish is an increasingly utilized approach to mitigate endemic infectious disease in aquaculture. In domesticated salmonid populations, large phenotypic variation in disease resistance has been identified but the genetic basis for altered responsiveness remains unclear. We previously reported three generations of selection and phenotypic validation of a bacterial cold water disease (BCWD) resistant line of rainbow trout, designated ARS-Fp-R. This line has higher survival after infection by either standardized laboratory challenge or natural challenge as compared to two reference lines, designated ARS-Fp-C (control) and ARS-Fp-S (susceptible). In this study, we utilized 1.1 g fry from the three genetic lines and performed RNA-seq to measure transcript abundance from the whole body of naive and Flavobacterium psychrophilum infected fish at day 1 (early time-point) and at day 5 post-challenge (onset of mortality). Sequences from 24 libraries were mapped onto the rainbow trout genome reference transcriptome of 46,585 predicted protein coding mRNAs that included 2633 putative immune-relevant gene transcripts. A total of 1884 genes (4.0% genome) exhibited differential transcript abundance between infected and mock-challenged fish (FDR < 0.05) that included chemokines, complement components, tnf receptor superfamily members, interleukins, nod-like receptor family members, and genes involved in metabolism and wound healing. The largest number of differentially expressed genes occurred on day 5 post-infection between naive and challenged ARS-Fp-S line fish correlating with high bacterial load. After excluding the effect of infection, we identified 21 differentially expressed genes between the three genetic lines. In summary, these data indicate global transcriptome differences between genetic lines of naive animals as well as differentially regulated transcriptional responses to infection.

Host-parasite genotypic interactions in the honey bee: the dynamics of diversity.

Parasites are thought to be a major driving force shaping genetic variation in their host, and are suggested to be a significant reason for the maintenance of sexual reproduction. A leading hypothesis for the occurrence of multiple mating (polyandry) in social insects is that the genetic diversity generated within-colonies through this behavior promotes disease resistance. This benefit is likely to be particularly significant when colonies are exposed to multiple species and strains of parasites, but host–parasite genotypic interactions in social insects are little known. We investigated this using honey bees, which are naturally polyandrous and consequently produce genetically diverse colonies containing multiple genotypes (patrilines), and which are also known to host multiple strains of various parasite species. We found that host genotypes differed significantly in their resistance to different strains of the obligate fungal parasite that causes chalkbrood disease, while genotypic variation in resistance to the facultative fungal parasite that causes stonebrood disease was less pronounced. Our results show that genetic variation in disease resistance depends in part on the parasite genotype, as well as species, with the latter most likely relating to differences in parasite life history and host–parasite coevolution. Our results suggest that the selection pressure from genetically diverse parasites might be an important driving force in the evolution of polyandry, a mechanism that generates significant genetic diversity in social insects.

Susceptibility to Teratosphaeria nubilosa and precocity of vegetative phase change in Eucalyptus globulus and E. maidenii (Myrtaceae)

Since the first report of Teratosphaeria nubilosa (Cooke) Crous &amp; U.Braun in Uruguay in 2007, young plantations of Eucalyptus globulus Labill. and E. maidenii F.Muell. have been severely damaged by Mycosphaerella leaf disease. The genetic variation in disease resistance and in the timing of heteroblastic phase change was examined in 194 open-pollinated families of E. globulus and 86 families of E. maidenii growing in a field trial in south-eastern Uruguay, naturally infected by T. nubilosa. Disease severity, precocity of vegetative phase change and tree growth were assessed at 14 months. E. globulus was significantly more susceptible to T. nubilosa than was E. maidenii, presenting higher severity of leaf spots (10.6% and 5.6%, respectively), higher defoliation (31.9% and 22.9%, respectively) and higher crown-damage index (39.1% and 27.4%, respectively). However, the heteroblastic transition began significantly earlier in E. globulus than in E. maidenii, with 34.1% and 2.8% of the trees having some proportion of their crown with adult foliage at 14 months, respectively. Significant individual narrow-sense heritabilities were found in E. globulus for severity of leaf spots (0.40), defoliation (0.24), crown-damage index (0.30) and proportion of adult foliage (0.64). Additive genetic variation in E. maidenii was significant only for defoliation and crown-damage index, with a moderate heritability (0.21 and 0.20, respectively). Although E. maidenii was more resistant to T. nubilosa than was E. globulus, the degree of resistance was not enough to consider this species as an alternative to E. globulus for high-risk disease sites. In addition, the small genetic variability for resistance on the juvenile foliage and the late transition to adult foliage suggested that the chances for early selection in E. maidenii are quite limited. By contrast, the genetic variation in E. globulus clearly indicated that through selection for resistance of the juvenile foliage, and especially by selecting for early phase change, it is possible to obtain genetic stock suitable for sites with high risk of T. nubilosa infection.