35S]t-butylbicyclophosphorothionate binding sites in susceptible and cyclodiene-resistant houseflies.

4-aminobutyric acid (GABA)-gated chloride ion channels are important molecular targets for a number of polychlorocycloalkane compounds including cyclodiene insecticides. Previous radioligand binding studies have indicated that cyclodiene insecticides are potent inhibitors of [35S]t-butylbicyclophosphorothionate ([35S]TBPS) binding to housefly thorax and abdomen membranes. In the present study, a laboratory-reared, cyclodiene-resistant (CYW) housefly strain (Musca domestica) showed resistance to a number of cyclodiene insecticides. Specific, saturable [35S]TBPS binding was detected in thorax and abdomen membranes prepared from housefly strains susceptible (CSMA) and resistant (CYW) to cyclodienes. Scatchard analysis of [35S]TBPS binding data from CSMA and CYW membranes revealed no significant differences between the two strains in either the affinity (Kd) or the density (Bmax) of specific, saturable binding sites. There were no differences in the comparative effectiveness of a range of polychlorocycloalkanes, including cyclodiene insecticides, as inhibitors of specific [35S]TBPS binding to CSMA and CYW thorax and abdomen membranes. Therefore, if an alteration in target site is a mechanism for resistance to cyclodienes in the CYW strain, it is not readily measurable using [35S]TBPS.     

Reduced neuronal sensitivity to dieldrin and picrotoxinin in a cyclodiene-resistant strain of Drosophila melanogaster (Meigen).

Toxicological and neurophysiological studies were performed to characterize the resistance mechanism in a cyclodiene-resistant strain of Drosophila melanogaster (Maryland strain). Dieldrin had an LC50 of 0.058 ppm against the larvae of susceptible D. melanogaster (Oregon-R wild type) when formulated in the rearing media. The LC50 of the resistant Maryland strain was 10.8 ppm, giving a resistance ratio (LC50-Maryland/LC50-susceptible) of 186-fold. Suction electrode recordings were made from peripheral nerves of the larval central nervous system to test whether reduced nerve sensitivity played any role in the observed resistance. In susceptible preparations (n = 5), inhibition of nerve firing by 1 mM gamma-aminobutyric acid (GABA) was effectively antagonized within 3-10 min by 10 microM dieldrin. In contrast, 30 min incubations with 10 microM dieldrin had no effect on preparations from cyclodiene-resistant individuals (n = 5). Similarly, 10 microM picrotoxinin blocked GABA-dependent inhibition in susceptible nerve preparations (n = 3). In recordings from resistant insects (n = 4), picrotoxinin displayed either weak antagonism of GABA or hyperexcitation indistinguishable from susceptible preparations. These results demonstrate that cyclodiene resistance in the Maryland strain of D. melanogaster 1) is expressed in immature stages, 2) is present at the level of the nerve, and 3) extends to picrotoxinin, albeit at a reduced level compared with dieldrin. The possible role of an altered GABA receptor in this resistance is discussed.     

Abamectin resistance in strains of vegetable leafminer,Liriomyza sativae (Diptera: Agromyzidae) is linked to elevated glutathione S‐transferase activity

Abamectin resistance was selected in the vegetable leafminer, Liriomyza sativae (Blanchard) (Diptera: Agromyzidae) under laboratory conditions, and cross‐resistance patterns and possible resistance mechanisms in the abamectin‐resistant strains (AL‐R, AF‐R) were investigated. Compared with the susceptible strain (SS), strain AL‐R displayed 39‐fold resistance to abamectin after 20 selection cycles during 25 generations, and strain AF‐R exhibited 59‐fold resistance to abamectin after 16 selection cycles during 22 generations. No cross‐resistance to cyromazine was found in both abamectin‐resistant strains. However, we failed to select for cyromazine resistance in L. sativae under laboratory conditions by conducting 17 selection cycles during 22 generations. However, moderate levels of cross‐resistance to abamectin (6–9 fold) were observed in strains which received cyromazine treatments. Biochemical analysis showed that glutathione S‐transferase (GST) activity in both abamectin‐resistant strains (AL‐R, AF‐R) was significantly higher than in the susceptible strain (SS), suggesting metabolically driven resistance to abamectinin L. sativae. Recommendations of mixtures or rotation of cyromazine and abamectin should be considered carefully, as consecutive cyromazine treatments may select for low‐level cross‐resistance to abamectin.     

Efficacy of abamectin fed to German cockroaches (Dictyoptera: Blattellidae) resistant to pyrethroids

Ten field-collected strains of the German cockroach, Blattella germanica (L.), with varying levels of pyrethroid resistance were tested for possible cross-resistance to abamectin administered as a bait. The time-mortality method was used for comparison of response with a known susceptible strain in 10-d feeding experiments. Essentially no resistance to abamectin was found. Extensive feeding inhibition occurred after a few days, but the amount of abamectin consumed varied substantially from strain to strain. Abamectin may have considerable potential as a cockroach bait insecticide.     

A 36‐bp deletion in the alpha subunit of glutamate‐gated chloride channel contributes to abamectin resistance in Plutella xylostella

Diamondback moth (DBM), Plutella xylostella (L.) (Lepidoptera: Plutellidae), is one of the most destructive pests in Brassicaceae crops, such as Chinese cabbage (Brassica rapa L.). It is rapidly developing resistance to abamectin, the dominant insecticide utilized in controlling P. xylostella in China and other southeastern Asian countries. The target of abamectin, the alpha subunit of glutamate‐gated chloride channel (GluClα), is thought to be involved in the development of abamectin resistance in nematodes and insects. This study investigated variants of GluClα in both abamectin‐susceptible and resistant strains of P. xylostella. A comparison of the PxGluClα sequences revealed three variants, including a 63‐bp substitution, a 36‐bp deletion, and a 65‐bp insertion. The frequency of the 36‐bp deletion was much higher in the abamectin‐resistant strain compared to the susceptible strain, whereas the 63‐bp substitution and 65‐bp insertion showed no significant difference between the resistant and susceptible strains. The in vitro expression of PxGluClα (with or without the 36‐bp deletion) in Xenopus laevis (Daudin) oocytes indicated that PxGluClα with the 36‐bp deletion was less sensitive to both glutamate and abamectin compared to the wild‐type PxGluClα. These findings suggest that the variant 36‐bp deletion in PxGluClα may confer abamectin resistance in P. xylostella after continuous abamectin selection, providing new insights into the management of this pest and contributing to the development of new reagents for pest control.     

Abamectin resistance in Drosophila is related to increased expression of P-glycoprotein via the dEGFR and dAkt pathways

Many insects have evolved resistance to abamectin but the mechanisms involved in this resistance have not been well characterized. P-glycoprotein (P-gp), an ATP-dependent drug-efflux pump transmembrane protein, may be involved in abamectin resistance. We investigated the role of P-gp in abamectin (ABM) resistance in Drosophila using an ABM-resistant strain developed in the laboratory. A toxicity assay, Western blotting analysis and a vanadate-sensitive ATPase activity assay all demonstrated the existence of a direct relationship between P-gp expression and ABM resistance in these flies. Our observations indicate that P-gp levels in flies' heads were higher than in their thorax and abdomen, and that both P-gp levels and LC₅₀ values were higher in resistant than in susceptible and P-gp-deficient strains. In addition, P-gp levels in the blood–brain barrier (BBB) of resistant flies were higher than in susceptible and P-gp-deficient flies, which is further evidence that a high level of P-gp in the BBB is related to ABM resistance. Furthermore, we found greater expression of Drosophila EGFR (dEGFR) in the resistant strain than in the susceptible strain, and that the level of Drosophila Akt (dAkt) was much higher in resistant than in susceptible flies, whereas that in P-gp-deficient flies was very low. Compared to susceptible flies, P-gp levels in the resistant strain were markedly suppressed by the dEGFR and dAkt inhibitors lapatinib and wortmannin. These results suggest that the increased P-gp in resistant flies was regulated by the dEGFR and dAkt pathways and that increased expression of P-gp is an important component of ABM resistance in insects.     

The transfer of pyrethroid resistance resulting from crosses between resistant German cockroaches and susceptible Asian cockroaches

Crosses were made between the Asian cockroach,Blattella asahinai Mizukubo, and resistant strains of the German cockroach,B. germanica (L.), to assess the transfer of pyrethroid resistance to the progeny and to study the inheritance mechanism(s) involved. It was shown that the strain of Asian cockroaches studied was susceptible to four pyrethroids. F₁ progeny were essentially susceptible to the same compounds. Tests with F₂ progeny and those from backcrosses to the resistant parent indicated that the data for each pyrethroid fit an hypothesis of simple, autosomal, nearly completely recessive inheritance. The results are discussed from the standpoint of the impact of the Asian genome on the inheritance mechanism(s).     

Blocking actions of heptachlor at an insect central nervous system GABA receptor.

The actions of the polychlorocycloalkane insecticide heptachlor, and its epoxide metabolite, were examined on GABA receptors in insects and vertebrates. Electrophysiological experiments on the cell body of the cockroach (Periplaneta americana) fast coxal depressor motor neuron (Df), and GABA-activated 36Cl- uptake experiments on microsacs prepared from cockroach ventral nerve cords showed that both heptachlor and heptachlor epoxide blocked functional GABA receptors. The block appeared to be non-competitive and was voltage-independent over the membrane potential range -75 mV to -110 mV. There was no significant difference between the potencies of heptachlor and heptachlor epoxide in the functional assays for insect GABA receptors. Both compounds inhibited [35S]-t-butylbicyclophosphorothionate [( 35S]TBPS) binding in insects and vertebrates. The findings provide further evidence for block of an insect GABA receptor/Cl- channel by the cyclodiene class of polychlorocycloalkanes, and reveal differences in the insecticide-[35S]TBPS binding site interactions of insects and vertebrates.     

Putative polymerase chain reaction markers for insecticide resistance in the leafminer Liriomyza trifolii (Diptera: Agromyzidae) to cyromazine and abamectin

In this study, random amplified polymorphic DNA polymerase chain reaction (RAPD-PCR) was used to identify polymorphic genomic DNA that would discriminate among cyromazine-resistant, abamectin-resistant, and susceptible Liriomyza trifolii (Burgess) (Diptera: Agromyzidae) leafminers. Using a reference strain that was susceptible to both cyromazine and abamectin, and a cyromazine-resistant strain and an abamectin-resistant strain, 400 oligonucleotides were assayed using RAPD-PCR. We found that two oligonucleotides, B10 and G16, amplified unique bands in the cyromazine-resistant strain but not in the reference or abamectin-resistant strains. Three oligonucleotides, K04, J13, and I02, showed polymorphisms unique to the abamectin-resistant strain but not in the reference or cyromazine-resistant strain. Leaf dip bioassays and RAPD-PCR were performed on two additional reference strains, seven strains from commercial ornamental production greenhouses, and one field strain. The two reference strains were negative for the resistance-correlated oligonucleotides. Of the seven strains from ornamental greenhouses, leaf dip bioassays showed that five had some level of resistance to both abamectin and cyromazine, whereas two were susceptible. The field strain was susceptible to both cyromazine and abamectin. In RAPD-DNA analyses, the five strains with abamectin resistance were positive for the three abamectin resistance-correlated oligonucleotides K04, J13, and I02. In the cases of cyromazine resistance, the five strains with cyromazine resistance were positive for the two cyromazine resistance-correlated oligonucleotides B10 and G16. The field strain and two greenhouse strains that were susceptible in leaf dip bioassays were negative for all three abamectin resistance-correlated oligonucleotides. The field strain and one greenhouse strain were negative for the two cyromazine resistance-correlated oligonucleotides; however, one greenhouse strain that was susceptible to cyromazine in leaf dip bioassay tested positive for one of the cyromazine resistance-correlated oligonucleotides. This method can be used to quickly identify cyromazine resistance, abamectin resistance, or both in leafminers, enabling a grower to choose an effective insecticide for leafminer control in a timely manner.     

Insecticide resistance in populations of Tuta absoluta (Lepidoptera: Gelechiidae)

1 Control failures of insecticides used against the tomato leafminer Tuta absoluta (Meyrick) (Lepidoptera: Gelechiidae) in Brazil led to the investigation of the possible occurrence of resistance of this insect pest to abamectin, cartap, methamidophos and permethrin. 2 The insect populations were collected from seven sites in the states of Minas Gerais, Rio de Janeiro, and São Paulo. These populations were subjected to concentration–mortality bioassays using insecticide‐impregnated filter papers. 3 We were unable to obtain a single population which provided a susceptibility standard for all insecticides tested. Therefore, the resistance levels were estimated in relation to the most susceptible population to each insecticide. Resistance to abamectin and cartap were observed in all populations when compared with the susceptible standard population, with resistance ratios ranging from 5.2‐ to 9.4‐fold and from 2.2‐ to 21.9‐fold for abamectin and cartap, respectively. Resistance to permethrin was observed in five populations with resistance ratios ranging from 1.9‐ to 6.6‐fold, whereas resistance to methamidophos was observed in four populations with resistance ratios ranging from 2.6‐ to 4.2‐fold. 4 The long period and high frequency of use of these insecticides against this insect pest suggest that the evolution of insecticide resistance on them has been relatively slow. Alternatively, the phenomenon might be widespread among Brazilian populations of T. absoluta making the finding of suitable standard susceptible populations difficult and leading to an underestimation of the insecticide resistance levels in this pest. 5 Higher levels of resistance to abamectin, cartap and permethrin are correlated with greater use of these compounds by growers. This finding suggests that local variation in insecticide use was an important cause of variation in susceptibility.     

Behavioral and physiological resistance of the German cockroach to gel baits (Blattodea: Blattellidae)

A gel bait-resistant German cockroach, Blattella germanica (L.), strain Cincy was collected in Cincinnati, OH. This strain exhibited a high level of behavioral resistance to Avert (0.05% abamectin) and Maxforce FC (0.01% fipronil) gel baits. Topical application assays indicated moderate levels of physiological resistance of the Cincy strain to abamectin and fipronil. Resistance ratios (based on LD50 values from topical applications) to abamectin and fipronil were 2.5 and 8.7, respectively. The Cincy strain of had a significantly lower LD50 value to abamectin than a nonaverse field strain (Dorie) and similar LD50 values to fipronil as the Dorie strain. The aversion behavior (avoidance of gel baits) was therefore caused by food ingredients in the gel baits. The Cincy strain showed avoidance of agar containing fructose, glucose, maltose, and sucrose, which are phagostimulants to the laboratory strain. Modifications of the inert ingredients in the Maxforce FC gel bait significantly improved the efficacy against the Cincy strain. The Cincy strain produced significantly smaller oothecae and lower numbers of eggs in each egg capsule than the nonaverse Jwax and Dorie strains of cockroaches, suggesting fitness costs are associated with resistance.     

Toxicity of Acaricides to the Bulb Mite Rhizoglyphus Echinopus (Acari: Acaridae)

Using a continuous exposure technique, the toxicity of 35 compounds to the bulb mite, Rhizoglyphus echinopus (Fumouze and Robin) was examined after 48 h. Sixteen acaricides yielded an LC₅₀ of <1.0 mg cm². The highest toxicity was exhibited by cyclodiene GABA antagonists (dieldrin, endrin and aldrin), some organophosphate (chlorpyrifos, diazinon and azinphosethyl) and carbamate (carbofuran) anticholinesterases and a thiazolidine flubenzimine. Oxythioquinox, fenazaflor, fenazaquin and amitraz were less toxic than the cyclodienes, organophosphates and carbamates. The sodium channel agonists (DDT and pyrethroids) and several specific acaricides with other modes of action were inactive (LC₅₀ >11.0 mg cm^-2).     

Baseline susceptibility of persea mite (Acari: Tetranychidae) to abamectin and milbemectin in avocado groves in Southern California

Persea mite, Oligonychus perseae Tuttle, Baker, and Abatiello, susceptibility to abamectin and milbemectin was evaluated in 2003 to determine baseline susceptibility levels in avocado groves in San Diego and Ventura Counties (California, USA) where more than 70% of the state’s avocado production is concentrated. Milbemectin has yet to be used in avocado production in California and abamectin has been available for use since 1999. Baseline susceptibility ratios (in relation to the most susceptible population) of five persea mite field strains to milbemectin varied 2.1- to 2.8-fold at the LC₅₀ and LC₉₀, respectively. The susceptibility of seven field strains to abamectin varied slightly more (2.1- to 3.5-fold) with one strain subjected to seven sprays over the past 4 years showing slight but significant separation of LC₅₀ and LC₉₀’s from the most susceptible strain, which is suggestive of the early stages of resistance to this product. Based on these data, baseline susceptibility levels are proposed that might be used to monitor for future persea mite resistance to these chemicals as their use in California avocado production continues.     

Insecticide toxicity, synergism and resistance in the German cockroach (Dictyoptera: Blattellidae)

The toxicity of synergism of and resistance to insecticides in four strains of German cockroach, Blattella germanica (L.), were investigated. Toxicity of nine insecticides by topical application to the susceptible strain varied greater than 2,000-fold, with deltamethrin (LD50 = 0.004 micrograms per cockroach) and malathion (LD50 = 8.4 micrograms per cockroach) being the most and least toxic, respectively. Resistance to pyrethrins (9.5-fold) in the Kenly strain was unaffected by the synergists piperonyl butoxide (PBO) or S,S,S-tributylphosphorotrithioate (DEF), suggesting that the metabolism is not involved in this case. Malathion resistance in the Rutgers strain was suppressible with PBO, implicating oxidative metabolism as a resistance mechanism. The Ectiban-R strain was resistant to all the pyrethroids tested, and cypermethrin resistance was not suppressible with PBO or DEF. These findings support results of previous studies that indicated this train has a kdr-like mechanism. Bendiocarb resistance in both the Kenly and Rutgers strains was partially suppressed by either PBO or DEF, suggesting that oxidative and hydrolytic metabolism are involved in the resistance. Trends between the effects of the synergists on the susceptible versus resistant strains are discussed.     

Knockdown resistance to dichlorodiphenyl-trichloroethane and pyrethroid insecticides in the napts mutant of Drosophila melanogaster is correlated with reduced neuronal sensitivity

Resistance to pyrethroid insecticides and dichlorodiphenyltrichloroethane (DDT) was investigated in the nap^ts (no action potential, temperature sensitive) mutant of Drosophila melanogaster. In surface contact bioassays, the nap^ts strain showed threefold resistance to deltamethrin at the LC₅₀ level when compared to susceptible Canton-S flies. Cross-resistance was also observed to DDT and the pyrethroids NRDC 157 [3-phenoxybenzyl [1R,cis]-3-(2,2-dibromovinyl)-2,2-dimethylcyclopropanecarboxylate], fenfluthrin, and MTI-800 [1-(3-phenoxy-4-fluorophenyl)-4-(4-ethoxyphenyl)-4-methylpentane]. The onset of intoxication by pyrethroids in nap^ts flies was markedly delayed, a finding that is consistent with the existence of a resistance mechanism involving reduced neuronal sensitivity. Resistance at the level of the nerve was confirmed by electrophysiological recordings of spontaneous and evoked activity in the dorsolongitudinal flight muscles of poisoned flies. Preparations from nap^ts insects treated with fenfluthrin displayed longer latencies to the appearance of spontaneous activity and also an absence or reduction in burst discharges compared to equivalent preparations from susceptible individuals. These results are discussed in light of competing hypotheses concerning the mechanism underlying knockdown resistance and reduced nerve sensitivity in insects.     

Mode of action of atracotoxin at central and peripheral synapses of insects

These studies characterized the paralytic and neurophysiological effects of an atracotoxin (ACTX), from the Australian funnel web spider, Hadronyche versuta, and compared it to the established P/Q-type calcium channel blocker, -agatoxin-IVA (-Aga-IVA). ACTX-induced paralysis was of a spastic form in housefly (Musca domestica) larvae, but it was inactive on neuromuscular junction of housefly and tobacco budworm (Heliothis virescens). On cockroach (Periplaneta americana) cercal nerve–giant fiber synapse preparations, both toxins were effective blockers with potencies in the nanomolar range, but some spontaneous, high frequency trains of action potentials were observed with ACTX. In Drosophila melanogaster central nervous preparations, blockage of nerve firing occurred within 20 min when the nerve sheath was intact, demonstrating that the barrier could be breached by ACTX in vitro. There was a potent (pM) excitatory response to ACTX in this tissue, prior to the onset of block at higher concentrations. In contrast, -Aga-IVA was a pure blocker in both cockroach and Drosophila preparations. These studies demonstrate that central synaptic calcium channels underlie the action of ACTX. ACTX-dependent neuroexcitation has a number of possible mechanisms that warrant further study.     

Resistance to Bacillus thuringiensis Mediated by an ABC Transporter Mutation Increases Susceptibility to Toxins from Other Bacteria in an Invasive Insect

Evolution of pest resistance reduces the efficacy of insecticidal proteins from the gram-positive bacterium Bacillus thuringiensis (Bt) used widely in sprays and transgenic crops. Recent efforts to delay pest adaptation to Bt crops focus primarily on combinations of two or more Bt toxins that kill the same pest, but this approach is often compromised because resistance to one Bt toxin causes cross-resistance to others. Thus, integration of Bt toxins with alternative controls that do not exhibit such cross-resistance is urgently needed. The ideal scenario of negative cross-resistance, where selection for resistance to a Bt toxin increases susceptibility to alternative controls, has been elusive. Here we discovered that selection of the global crop pest, Helicoverpa armigera, for >1000-fold resistance to Bt toxin Cry1Ac increased susceptibility to abamectin and spineotram, insecticides derived from the soil bacteria Streptomyces avermitilis and Saccharopolyspora spinosa, respectively. Resistance to Cry1Ac did not affect susceptibility to the cyclodiene, organophospate, or pyrethroid insecticides tested. Whereas previous work demonstrated that the resistance to Cry1Ac in the strain analyzed here is conferred by a mutation disrupting an ATP-binding cassette protein named ABCC2, the new results show that increased susceptibility to abamectin is genetically linked with the same mutation. Moreover, RNAi silencing of HaABCC2 not only decreased susceptibility to Cry1Ac, it also increased susceptibility to abamectin. The mutation disrupting ABCC2 reduced removal of abamectin in live larvae and in transfected Hi5 cells. The results imply that negative cross-resistance occurs because the wild type ABCC2 protein plays a key role in conferring susceptibility to Cry1Ac and in decreasing susceptibility to abamectin. The negative cross-resistance between a Bt toxin and other bacterial insecticides reported here may facilitate more sustainable pest control.     

Multiple Origins of Cyclodiene Insecticide Resistance in Tribolium castaneum (Coleoptera: Tenebrionidae)

The number of origins of pesticide resistance-associated mutations is important not only to our understanding of the evolution of resistance but also in modeling its spread. Previous studies of amplified esterase genes in a highly dispersive Culex mosquito have suggested that insecticide resistance-associated mutations (specifically a single-gene duplication event) can occur a single time and then spread throughout global populations. In order to provide data for resistance-associated point mutations, which are more typical of pesticide mechanisms as a whole, we studied the number of independent origins of cyclodiene insecticide resistance in the red flour beetle Tribolium castaneum. Target-site insensitivity to cyclodienes is conferred by single point mutations in the gene Resistance to dieldrin (Rdl), which codes for a subunit of a γ-aminobutyric acid (GABA) receptor. These point mutations are associated with replacements of alanine 302 which render the receptor insensitive to block by the insecticide. We collected 141 strains of Tribolium worldwide and screened them for resistance. Twenty-four strains contained resistant individuals. After homozygosing 23 of these resistance alleles we derived a nucleotide sequence phylogeny of the resistant strains from a 694-bp section of Rdl, encompassing exon 7 (which contains the resistance-associated mutation) and part of a flanking intron. The phylogeny also included six susceptible alleles chosen at random from a range of geographical locations. Resistance alleles fell into six clades and three clades contained both resistant and susceptible alleles. Although statistical analysis provided support at only the 5–6% level, the pattern of variation in resistance alleles is more readily explained by multiple independent origins of resistance than by spread of a single resistance-associated mutation. For example, two resistance alleles differed from two susceptible alleles only by the resistance-associated mutation itself, suggesting that they form the susceptible ancestors and that resistance arose independently in several susceptible backgrounds. This suggests that in Tribolium Rdl, de novo mutations for resistance have arisen independently in several populations. Identical alleles were found in geographically distant regions as well, also implying that some Rdl alleles have been exported in stored grain. These differences from the Culex study may stem both from differences in the population genetics of Tribolium versus that of mosquitoes and differences in mutation rates associated with point mutations versus gene duplication events. The Tribolium data therefore suggest that multiple origins of insecticide resistance (associated with specific point mutations) may be more common than the spread of single events. These findings have implications for the way in which we model the evolution and spread of insecticide resistance genes and also suggest that parallel adaptive substitutions may not be uncommon in phyletic evolution. Received: 14 October 1998 / Accepted: 4 January 1999     

Sexual selection reveals a cost of pathogen resistance undetected in life-history assays

Mechanisms of resistance to pathogens and parasites are thought to be costly and thus to lead to evolutionary trade-offs between resistance and life-history traits expressed in the absence of the infective agents. On the other hand, sexually selected traits are often proposed to indicate “good genes” for resistance, which implies a positive genetic correlation between resistance and success in sexual selection. Here I show that experimental evolution of improved resistance to the intestinal pathogen Pseudomonas entomophila in Drosophila melanogaster was associated with a reduction in male sexual success. Males from four resistant populations achieved lower paternity than males from four susceptible control populations in competition with males from a competitor strain, indicating an evolutionary cost of resistance in terms of mating success and/or sperm competition. In contrast, no costs were found in larval viability, larval competitive ability and population productivity assayed under nutritional limitation; together with earlier studies this suggests that the costs of P. entomophila resistance for nonsexual fitness components are negligible. Thus, rather than indicating heritable pathogen resistance, sexually selected traits expressed in the absence of pathogens may be sensitive to costs of resistance, even if no such costs are detected in other fitness traits.