Additive Genetic Variation In Resistance Research Articles

Additive genetic variation in resistance of Nile tilapia (Oreochromis niloticus) to Francisella orientalis and its genetic (co)variation to both harvest weight and resistance to Streptococcus agalactiae Ib

An understanding of the genetic relationship between traits of economic importance for a widely cultured species such as Nile tilapia (Oreochromis niloticus) is important, in particular the relationship between disease resistance and growth. Francisellosis results in economic losses for the industry, and we confirmed that Francisellosis resistance is under additive genetic control in our population. Analysing four generations, significant additive genetic variation was found for survival to F. orientalis challenge (P < 0.001; Log-likelihood-ratio test) with an estimated heritability of h2 = 0.31 ± 0.05 across all generations. The random effect common to full-sibs was also significant, but of lower magnitude (c2 = 0.075 ± 0.02) (P < 0.001; Log-likelihood-ratio test). Results of assortative mating groups confirmed that genetic gain could be obtained for survival to F. orientalis challenge since offspring of fish selected with high estimated breeding values exhibited higher survival to F. orientalis challenge. The genetic correlation between harvest weight and survival to F. orientalis challenge was very low (rg = −0.02 ± 0.13) and not significantly different from zero (Log-likelihood-ratio test p > 0.05). The genetic correlation between survival to F. orientalis challenge and survival to S. agalactiae Ib challenge was positive but not significantly different from zero (rg = 0.14 ± 0.11; Log-likelihood-ratio test p > 0.05). The genetic correlation between harvest weight and survival to S. agalactiae challenge was negative but also not significantly different (rg = − 0.19 ± 0.10; Log-likelihood-ratio test p > 0.05). Lack of significant favourable genetic relationships between economically important traits favours multi-trait selection since selection for growth alone does not improve survival to F. orientalis challenge or survival to S. agalactiae challenge.

On the trail of detecting genetic (co)variation between resistance to parasite infections (Diplectanum aequans and Lernanthropus kroyeri) and growth in European seabass (Dicentrarchus labrax)

The European seabass is one of the main commercial fish produced in Mediterranean marine aquaculture. Recently, its production has been negatively affected by losses due to frequent and recurring outbreaks of parasitic, bacterial and viral diseases. In recent years, the gill parasites Diplectanum aequans and Lernanthropus kroyeri are increasingly becoming more dominant and contributing more significantly to the observed losses. Genetic improvement for disease resistance represents an important strategy for controlling infectious diseases in farmed fish by increasing their robustness. In order to determine the possibility of including such trait in selective breeding programs, we need to comprehend whether additive genetic variation for resistance against Diplectanum aequans and Lernanthropus kroyeri exists. For this purpose, two open-sea parasite cohabitation trials (for two consecutive years) were performed in the commercial production sites of a private company (Nireus S.A), that had high infestation with Diplectanum aequans and Lernanthropus kroyeri. Juvenile European seabass (9425 offspring from 91 full-sib and half-sib families per year), originating from the company's breeding program were equally divided into two groups and transferred to two commercial farming sites located in the areas of Nafpactos and Sagiada, in western Greece, for the intended cohabitation studies. The parasite numbers on all the gill arches were counted and recorded at the end of the trials for the infestation levels. A third site (Palairos) without any parasite infestation was used as a control site. A multi-trait animal model was used to estimate the variance-covariance components and to evaluate the genetic parameters for Parasite Counts, recorded from all the gill arches of the fish, and their corresponding growth in sea cages. The estimated heritabilities for parasite count, using untransformed data, were 0.20 (D. aequans) and 0.28 (L. kroyeri) and for transformed data 0.29 and 0.26, respectively. The heritability estimates for body weight were 0.42−0.51 for D. aequans and 0.28−0.51 for L. kroyeri trials. Similarly, estimated heritabilities for the growth in sea cages were 0.43 and 0.29, respectively. Although parasite count has a low to medium unfavorable genetic correlation with body weight and growth (0.09−0.37), it seems that it is not significantly impairing selection for growth. Furthermore, the results of this study are very promising in terms of the existing potential for genetic improvement of parasite resistance, and provides a good basis for further genetic analysis using molecular markers.

Resistance to Streptococcus iniae and its genetic associations with traits of economic importance in Asian seabass (Lates calcarifer).

Streptococcus iniae is one of the most serious aquatic pathogens, causing significant economic losses in marine and freshwater species, including Asian seabass (Lates calcarifer). Controlling this gram-positive bacterial pathogen has been an issue in aquaculture systems, due to the combined effects of aquaculture intensification and climatic impacts. To date, there have not been any genetic parameter estimates for S.iniae resistance in Asian seabass. The main aim of this study was to examine genetic variation in S.iniae resistance and its genetic correlations with growth and cannibalism in Asian seabass families produced from a breeding programme for high growth in 2016 and 2017. The study included a total of 5,835 individual fish that were offspring of 41 sires and 60 dams (31 half-sib and 34 full-sib families). The experimental fish were challenged by intraperitoneal injection with a volume containing 105 CFU (colony-forming unit)/fish. Resistance to S.iniae was measured as survival rate at 6hr, 3, 5, 7, 10 and 15days post-challenge test. There were significant variations in S.iniae resistance among families at different observation periods (ranging from 24.4% to 80%). Restricted maximum-likelihood method and mixed model analysis were applied to estimate heritability for S.iniae resistance. The heritability for S.iniae resistance ranged from 7% to 18% across different statistical models used. The common full-sib effects accounted for 0.1%-2% of the total variation in resistance to S.iniae. Genetic correlations of the S.iniae resistance at 6hr and 3days with later post-challenge test periods were low to moderate. However, these estimates for S.iniae resistance between successive measurement times (5, 7, 10 and 15days) were high and close to 1. The genetic correlations of resistance with body weights at 180, 270 and 360days post-hatch were not significant as well with cannibalism. It is concluded that there is substantial additive genetic variation in resistance to S.iniae, suggesting there is potential for genetic improvement of Asian seabass for resistance to S.iniae through selective breeding.

Quantitative genetics of disease resistance in different groups of Penaeus semisulcatus from preliminary controlled challenge test with Vibrio parahaemolyticus the aetiological agent of acute hepatopancreatic necrosis disease (AHPND)

ABSTRACTAcute hepatopancreatic necrosis disease (AHPND) has caused losses to shrimp farmers worldwide owing to Vibrio parahaemolyticus (VPAHPND). Selective breeding for disease resistance of shrimp was used as an alternative strategy for disease control. Five subsamples of shrimp from 20 full-sib families were subjected to a cohabitation challenge test. Juveniles of P. semisulcatus (mean weight 2.5 ± 0.17 g) were tested for survival after challenge with VPAHPND. Mortality in the challenge test was recorded daily, and the experiment was terminated after 96 days when the mortality ceased. Moderate heritabilities were estimated in resistance to VPAHPND based on a linear model (LM) and threshold model (TM). This indicates that disease resistance is a heritable trait, and a challenge test may serve as a basis for selection for resistance to VPAHPND in P. semisulcatus. However, further investigation is needed to confirm and quantify the additive genetic variation for resistance to VPAHPND in P. semisulcatus.

First insight into the heritable variation of the resistance to infection with the bacteria causing the withering syndrome disease in Haliotis rufescens abalone.

Withering syndrome disease has experienced worldwide spread in the last decade. This fatal disease for abalone is produced by a rickettsia-like organism (WS-RLO), the bacterium "Candidatus Xenohaliotis californiensis". To evaluate the potential of the red abalone (Haliotis rufescens) to improve its resistance to infection by WS-RLO, the additive genetic component in the variation of this trait was estimated. For this, the variation in infection intensity with WS-RLOs and WS-RLOv (phage-infected RLOs) was analyzed in 56 families of full-sibs maintained for three years in a host-parasite cohabitation aquaculture system. A WS-RLO prevalence of 65% was observed in the analysed population; and from the total WS-RLO inclusions 60% were hyperparasited with the phage (WS-RLOv). The decrease in the food ingestion rate was the sole negative effect associated with increasing WS-RLO intensity of infection, suggesting that the high level of WS-RLOv load may have diminished the symptoms of WS disease in the analyzed abalones. The estimated heritabilities were moderate to mid, but significant, varying from 0.21 to 0.23 and 0.36 for WS-RLO and WS-RLOv infections, respectively. This suggests that variation in resistance to infection with WS-RLO may respond to selection in the evaluated red abalone population. Estimated response to selection (G) for the level of infection by WS-RLO indicated that if the 10% of red abalone with the lowest infection level is selected as broodstock, a 90% reduction in the intensity of infection in the progeny can be expected, even with the lowest estimation of heritability (h2=0.21). This strong response would be also due to the large phenotypic variance of this trait. Strong positive correlations, both phenotypic and genotypic, were observed between infection intensities with WS-RLO and WS-RLOv, indicating that selection to increase resistance to one of the types of RLOs will affect resistance in the other in the same direction. This is the first study that demonstrates the existence of additive genetic variation for resistance to WS-RLO in abalone. Consequently, it is possible to increase the resistance to WS-RLO in H. rufescens by selective breeding, which can be an economically attractive and environmentally friendly manner to reduce mortalities and growth effects caused by WS in abalone farms.

Additive genetic variation in resistance of Nile tilapia (Oreochromis niloticus) to Streptococcus iniae and S. agalactiae capsular type Ib: Is genetic resistance correlated?

Streptococcus iniae and S. agalactiae are both economically important Gram positive bacterial pathogens affecting the globally farmed tilapia (Oreochromis spp.). Historically, control of these bacteria in tilapia culture has included biosecurity, therapeutants and vaccination strategies. Genetic gains in performance traits have been realized for Nile tilapia (Oreochromis niloticus) and interest in breeding for disease resistance has recently received attention. The goal of this study was three fold: 1) to verify previous results demonstrating heritability of S. iniae resistance in Nile tilapia families using increased numbers of fish per family; 2) to determine if realized genetic gain in resistance and/or susceptibility to S. iniae can be obtained following positive assortative mating between parents with high or low estimated breeding values (EBV); and 3) to determine if resistance to S. iniae and S. agalactiae capsular type Ib is genetically correlated. A total of 144 and 130 full sib families were challenged intraperitoneally with S. iniae and intramuscularly with S. agalactiae Ib, respectively. Cumulative mortality at test end was 46% for S. iniae and 68% for S. agalactiae. There was a high additive genetic component found for survival in fish injected with S. iniae (estimated heritability 0.52±0.12) and with S. agalactiae (estimated heritability 0.38±0.11). The S. iniae challenge results confirmed additive genetic variation in resistance of Nile tilapia to S. iniae. We also demonstrated via assortative mating that genetic gain for survival to S. iniae is possible. The genetic correlation between resistance to S. iniae and S. agalactiae Ib was not significantly different from zero (rg=−0.30±0.19). The lack of correlation suggests if resistance to both Streptococcus sp. is desired, selection for both traits must be simultaneous. Selection of fish to improve survival to Streptococcus sp. may require a thorough understanding of the type of pathogen prevalent in the region so that custom genetic material may be tailored to meet the needs of the individual farm and/or region.

Controlled challenge experiment demonstrates substantial additive genetic variation in resistance of Nile tilapia (Oreochromis niloticus) to Streptococcus iniae

Streptococcus iniae is an etiologic agent of streptococcal disease in tilapia and is one of several Streptococcus spp. that negatively impact worldwide tilapia production. Methods for the prevention and control of S. iniae include vaccines, management strategies, and antibiotics. A complimentary preventative approach may include selective breeding for disease resistance, but the potential for this is unknown in tilapia. This study was initiated to challenge Nile tilapia (Oreochromis niloticus) families for estimation of genetic parameters for resistance to S. iniae. A total of 143 full- and paternal half-sib families (avg. 176g, sd=50g) were divided into two groups with each containing on average 9 fish per family. The challenge was designed with the intent to utilize fish injected with S. iniae (Group 1) as shedder fish to transfer the bacterium to cohabitated fish (Group 2). Tilapia from Group 1 were challenged by intraperitoneal injection with a volume containing 1.15×108 colony-forming units S. iniae per fish, and then cohabitated with tilapia from Group 2 in a single tank. Accumulated mortality at the end of the experiment was 60% for the fish challenged by injection and 6.4% for fish challenged by cohabitation. The results revealed high variation for mean survival of the families injected with S. iniae (range from 0% to 100%, CV 69%). The estimated heritability of post-challenge survival in Group 1 was 0.42±0.07 on the observed binary scale and 0.58±0.09 on the underlying liability scale, derived from fitting a linear animal model and a sire-dam threshold model, respectively. In summary, substantial additive genetic variation in resistance to S. iniae was observed when fish were challenged by injection, and this suggests promise for genetic improvement of tilapia for resistance to S. iniae through selective breeding. Statement of relevanceThis research suggests promise for genetic improvement of tilapia for resistance to Streptococcus iniae through selective breeding, thereby providing commercial fish farmers with a more resistant stock of tilapia as an additional management tool for reducing production losses due to Streptococcus spp.

New Insight for the Genetic Evaluation of Resistance to Ostreid Herpesvirus Infection, a Worldwide Disease, in Crassostrea gigas.

The Pacific oyster, Crassostrea gigas, is the most important commercial oyster species cultivated in the world. Meanwhile, the ostreid herpesvirus 1 (OsHV-1) is one of the major pathogens affecting the Pacific oyster, and numerous mortality outbreaks related to this pathogen are now reported worldwide. To assess the genetic basis of resistance to OsHV-1 infection in spat C. gigas and to facilitate breeding programs for such a trait, if any exist, we compared the mortality of half- and full-sib families using three field methods and a controlled challenge by OsHV-1 in the laboratory. In the field, three methods were tested: (A) one family per bag; (B) one family per small soft mesh bag and all families inside one bag; (C) same as the previous methods but the oysters were individually labelled and then mixed. The mean mortality ranged from 80 to 82% and was related to OsHV-1 based on viral DNA detection. The narrow-sense heritability for mortality, and thus OsHV-1 resistance, ranged from 0.49 to 0.60. The high positive genetic correlations across the field methods suggested no genotype by environment interaction. Ideally, selective breeding could use method B, which is less time- and space-consuming. The narrow sense heritability for mortality under OsHV-1 challenge was 0.61, and genetic correlation between the field and the laboratory was ranged from 0.68 to 0.75, suggesting a weak genotype by environment interaction. Thus, most of families showing the highest survival performed well in field and laboratory conditions, and a similar trend was also observed for families with the lowest survival. In conclusion, this is the first study demonstrating a large additive genetic variation for resistance to OsHV-1 infection in C. gigas, regardless of the methods used, which should help in selective breeding to improve resistance to viral infection in C. gigas.

Estimates of genetic variation in the susceptibility of Atlantic salmon ( Salmo salar) to the salmon louse Lepeophtheirus salmonis

The magnitude of the genetic variation in the susceptibility of Atlantic salmon to Lepeophtheirus salmonis was estimated through a controlled infestation test of 2206 individually tagged post-smolts of 154 full-sib families, i.e. the offspring of 78 sires and 154 dams. The infestation test took place in two replicated tanks with seawater. On average 74 and 36 copepodids per fish were added to tanks 1 and 2, respectively. The number of sessile lice (chalimus II–II stage) per fish (LC) was counted ten days after infestation at which the average body weight of the fish was 260 g in each of the two tanks. The average LC per fish was 27.1 (SD = 16.4) and 13.9 (SD = 13.2) in tanks 1 and 2, respectively while the lice density per fish, calculated as LD = LC/Body weight 2/3, was 0.66 (SD = 0.38) and 0.34 (SD = 0.29). Observed LC was found to increase with increasing body weight, while LD was seemingly independent of body weight. These relationships explain the lower heritability for LD (0.26 ± 0.05) than for LC (0.33 ± 0.05), and a genetic correlation between LC and LD (r g = 0.89 ± 0.03) different from unity. The magnitude of the heritability estimate for LD together with the large phenotypic variation of the trait, and a genetic correlation close to unity between LD in the two replicated tanks, shows that there is substantial additive genetic variation in resistance to L. salmonis in Atlantic salmon, and thus a great potential for increasing the resistance through selective breeding. The genetic correlation between LD and harvest body weight recorded on two subsamples of sibs of the lice infected fish reared at two farms was close to and not significantly different from zero (0.06 ± 0.12 and − 0.13 ± 0.11). Hence, the increasing lice problem in the salmon industry during the last years is most likely caused by other factors than the selection that has been practised for increased growth rate over the last 3–4 decades.

Selective breeding provides an approach to increase resistance of rainbow trout ( Onchorhynchus mykiss) to the diseases, enteric redmouth disease, rainbow trout fry syndrome, and viral haemorrhagic septicaemia

In this study, we reasoned that if we challenged rainbow trout with the causative agents of enteric redmouth disease (ERM), rainbow trout fry syndrome (RTFS), and viral haemorrhagic septicaemia (VHS), we would: 1) detect additive genetic variation for resistance to ERM, RTFS, and VHS; and 2) find that resistance of the trout to ERM and RTFS are favourably correlated genetically, while resistance to VHS is unfavourably correlated with resistance to ERM and RTFS. We tested these premises by challenging 63 full-sib families of rainbow trout (50 sires, 38 dams) with Yersinia ruckeri, Flavobacterium psychrophilum, and VHS virus, the causative agents of ERM, RTFS, and VHS. Resistance to each disease was assessed as both a binary trait (i.e., died/survived) and a longitudinal trait (i.e., time until death following challenge). Additive genetic variation and genetic correlations for resistance to ERM, RTFS, and VHS were estimated by fitting a threshold liability model to resistance assessed as a binary trait. As a longitudinal trait, additive genetic variation and genetic correlations were estimated by fitting a Weibull frailty model to the times until death. Our findings support the first of our premises as we detected additive genetic variation for resistance to ERM, RTFS, and VHS. The heritability for resistance to ERM, RTFS, and VHS ranged between 0.42 and 0.57 on the underlying liability scale when resistance was assessed as a binary trait. As a longitudinal trait, the heritabilities ranged between 0.07 and 0.21 for time until death on the logarithmic-time scale. We were, however, unable to support our second premise as we found that resistance to each of the diseases tended to be weakly correlated genetically. The genetic correlations between the resistances ranged between −0.11 and 0.15 when resistance was assessed as a binary trait, and between −0.23 and 0.16 when resistance was assessed as a longitudinal trait. These findings are encouraging for commercial trout production. The additive genetic variation detected for resistance demonstrates that selectively breeding trout for resistance to ERM, RTFS, and VHS will be successful, providing a complementary approach to control these diseases. The weak genetic correlations suggest that it should be relatively easy to improve resistance to each of the diseases simultaneously.

Heritability of resistance against ectoparasitism in the Drosophila–Macrocheles system

Ectoparasites are abundant in natural communities, can have pronounced deleterious fitness consequences to their host and are important vectors of transmissible parasitic disease. Yet very few studies have estimated the magnitude of heritable genetic variation underlying resistance against ectoparasitism, which significantly limits our ability to predict the evolution of this ecologically important character. The present paper reports results of artificial selection for increased resistance in Drosophila nigrospiracula against ectoparasitic, haematophagous mites, Macrocheles subbadius. In this system, which occurs naturally in the Sonoran Desert of North America, ectoparasitism significantly damages the expression of host fitness traits, including longevity, fecundity and male mating success. In the present study, resistance, which was modelled as a threshold trait, responded significantly to selection applied on either sex. Realized heritability, calculated as a mean across four replicates, was estimated to be 0.152 +/- 0.014 (SE). The heritability estimate from selection on males did not differ from that on females, but both estimates differed significantly from zero. This documented presence of additive genetic variation for resistance, coupled with knowledge of the fitness consequences of ectoparasitism, indicates that the host population possesses significant evolutionary potential. Selection was applied on the pre-attachment phase, thereby targeting behavioural forms of defence. This study therefore establishes parallels between insects and other animals in their ability to protect themselves and evolve behavioural defences against ectoparasites.

Genetic variation for resistance to clinical and subclinical diseases exists in growing pigs

AbstractThe objective of this study was to test that genetic variation for resistance to clinical and subclinical diseases exists in growing pigs. A total of 13 551 male growing pigs were assessed for resistance to five categories of clinical and subclinical disease: (i) any clinical or subclinical disease, (ii) lameness, (iii) respiratory diseases, (iv) diarrhoea, and (v) other diseases (i.e. any clinical or subclinical disease with the exception of (ii), (iii), and (iv)). Additive genetic variation for resistance to each disease category was estimated by fitting a Weibull, sire-dam frailty model to time until the pigs were first diagnosed with a disease from that category. Genetic correlations among the resistances to each disease category were approximated as product-moment correlations among predicted breeding values of the sires. Additive genetic variation was detected for resistance to (i) any clinical or subclinical disease (additive genetic variance for log-frailty (± s.e.) = 0·18 ± 0·05, heritability on the logarithmic-time scale = 0·10), (ii) lameness (0·29 ± 0·11, 0·16), (iii) respiratory diseases (0·24 ± 0·16, 0·12), (iv) diarrhoea (0·30 ± 0·27, 0·16), and (v) the other diseases (0·34 ± 0·15, 0·19) and there were generally positive and low-to-moderate correlations among the predicted breeding values (-0·03 to + 0·65). These results demonstrate that additive genetic variation for resistance to clinical and subclinical diseases does exist in growing pigs, and suggests that selective breeding for resistance could be successful.

Selection for fenpropathrin and fenpropathrin + acephate resistance in the silverleaf whitefly (Homoptera: Aleyrodidae).

A large, genetically diverse pool of Bemisia argentifolii Bellows & Perring was collected in 1994 from different crops, and a mixed colony was established in the laboratory. Subsets of this colony were reared on cotton plants held in large Plexiglas cages, and adult whiteflies were selected for resistance to fenpropathrin and to fenpropathrin + acephate (1:5). Selection was performed by exposing adults to treated glass vials at doses sufficient to give 60-80% mortality. Thirteen generations of adult selection with fenpropathrin + acephate yielded 856.3- and 1,289.3-fold tolerance (using lethal concentration ratio), respectively, to fenpropathrin and to fenpropathrin + acephate, indicating additive genetic variation for resistance in the source population. Selection with fenpropathrin alone yielded only a 10.9-fold increase in tolerance to fenpropathrin at the end of the selection period. There was no significant change in tolerance to fenpropathrin + acephate in this strain. Contrary to expectations, the early onset and the magnitude of resistance attained on selection with fenpropathrin + acephate compared with fenpropathrin alone indicates that this mixture evidently possesses a high degree of selectivity for development of resistance in B. argentifolii. Estimates of realized heritability of resistance to fenpropathrin and to fenpropathrin + acephate in B. argentifolii (in the fenpropathrin + acephate-selected strain) showed that they were significantly higher in the first half of selection (six generations), in both instances. Rearing of the fenpropathrin + acephate-resistant strain under conditions free of insecticides for six generations did not result in any significant decline in resistance, indicating that resistance is fairly stable.

Heritable variation in resistance to gastro-intestinal nematodes in an unmanaged mammal population.

The impact of parasites on natural populations has received considerable attention from evolutionary biologists in recent years. Central to a number of theoretical developments during this period is the assumption of additive genetic variation in resistance to parasites. However, very few studies have estimated the heritability of parasite resistance under field conditions, and those that have are mainly restricted to birds and their ectoparasites. In this paper, to our knowledge, we show for the first time in a free-ranging mammal population, Soay sheep (Ovis aries) living on the islands of St Kilda, that there is significant heritable variation in resistance to gastrointestinal nematodes. This result is consistent with earlier studies on this population which have indicated locus-specific associations with parasite resistance. We discuss our results in the context of current studies examining heritable resistance to parasites in domestic sheep and the possible mechanisms of selective maintenance of genetic variation for resistance to gastrointestinal nematodes in the St Kilda Soay sheep population.

A model for the coevolution of resistance and virulence in coupled host–parasitoid interactions

A coevolutionary model is developed of the interaction between a host and an internal parasitoid, where the outcome of parasitism depends upon the extent to which individual hosts invest in resistance mechanisms and individual parasitoids in countermeasures (virulence). The host and parasitoid are assumed to have coupled population dynamics (of Nicholson–Bailey form) and to be composed of a series of asexual clones with different levels of resistance and virulence. Investment in resistance and virulence mechanisms is assumed to be costly. The model has two main outcomes. First, if resistance is relatively costly compared to virulence, the host may be selected not to invest in resistance mechanisms despite parasitoid investment in virulence, in effect trading off the risks of parasitism against the savings in costs. A number of cases which appear to correspond to this result have been reported. Second, for most other feasible parameter values, an arms race occurs between host and parasitoid, until effective resistance becomes so costly that the host abandons defence. This abandonment is followed by a reduction in parasitoid virulence and the cycle begins again. These cycles may explain reports of persistent additive genetic variation in resistance and virulence, and may also contribute towards population dynamic stability.

Trade-off associated with selection for increased ability to resist parasitoid attack in Drosophila melanogaster.

Costs of resistance are widely assumed to be important in the evolution of parasite and pathogen defence in animals, but they have been demonstrated experimentally on very few occasions. Endoparasitoids are insects whose larvae develop inside the bodies of other insects where they defend themselves from attack by their hosts' immune systems (especially cellular encapsulation). Working with Drosophila melanogaster and its endoparasitoid Leptopilina boulardi, we selected for increased resistance in four replicate populations of flies. The percentage of flies surviving attack increased from about 0.5% to between 40% and 50% in five generations, revealing substantial additive genetic variation in resistance in the field population from which our culture was established. In comparison with four control lines, flies from selected lines suffered from lower larval survival under conditions of moderate to severe intraspecific competition.

Seed predation, pathogen infection and life-history traits in Brassica rapa.

Herbivory and disease can shape the evolution of plant populations, but their joint effects are rarely investigated. Families of plants of Brassica rapa (Brassicaceae) were grown from seeds collected in two naturalized populations in an experimental garden. We examined leaf infection by the fungus Alternaria, seed predation by a gall midge (Cecidomyiidae) and plant life-history traits. Plants from one population had heavier seeds, were more likely to flower, had less fungal infection, had more seed predation and were more fecund. Fungal infection score and seed predation rate increased with plant size, but large plants still had the greatest number of undamaged fruits. Spatial heterogeneity in the experimental garden was significant; seed predation rate and fecundity varied among blocks. An apparent tradeoff existed between susceptibility to disease and seed predation: plants with the highest fungal infection score had the lowest seed predation rate. Alternaria infection varied between populations, but the disease had no effect on fecundity. Seed predation did reduce fecundity. Damaged fruits had 31.4% fewer intact seeds. However, evidence for additive genetic variation in resistance to seed predation was weak. Therefore, neither disease nor seed predation was likely to be a strong agent of genetically based fecundity selection.

Quantitative Genetic Tools for Insecticide Resistance Risk Assessment: Estimating the Heritability of Resistance

Quantitative genetic studies of resistance can provide estimates of genetic parameters not available with other types of genetic analyses. Three methods are discussed for estimating the amount of additive genetic variation in resistance to individual insecticides and subsequent estimation of the heritability (h2) of resistance. Sibling analysis and offspring-parent regression permit direct estimates of h2 by comparing the resistance phenotypes of individuals of known relatedness. Threshold trait analyses, performed on data from selection experiments, provide estimates of realized heritability. Procedures are outlined for predicting changes in resistance to insecticides based on h2 estimates. Quantitative genetic theory is examined as it relates to resistance and resistance as a quantitative trait; quantitative genetic methods also are unique in providing estimates of genetic correlations between traits. Comments are included on estimates of genetic correlation between resistance and phenotypic traits (e.g., development time) and how they may be used to predict changes in the genetic aspects of phenology that result from insecticide applications (i.e., to predict how the reproductive capacity of future generations will differ from that of the treated generation).