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Despite substantial costs, biparental sex is the dominant mode of reproduction across plant and animal taxa. The Red Queen hypothesis (RQH) posits that coevolutionary interactions with parasites can favor biparental sex in hosts, despite the costs. In support of the RQH, previous studies found that coevolutionary interactions with virulent bacterial parasites maintained high outcrossing rates in populations of the androdioecious nematode host Caenorhabditis elegans . Here we test three non-mutually exclusive mechanisms that could explain how coevolving parasites maintain outcrossing rates in C. elegans hosts: 1) short-term parasite exposure induces plastic increases in the hosts' propensity to outcross, 2) hosts evolve increased outcrossing propensity in response to selection imposed by coevolving parasites, and 3) outcrossed offspring incur less parasite-mediated fitness loss than selfed offspring, increasing host male frequencies and opportunities for outcrossing. We find no evidence that parasites cause plastic or evolved changes in host outcrossing propensity. However, parental outcrossing significantly increases survival of host offspring in the F2 generation when exposed to a coevolving parasite. Hence, coevolving parasites maintain outcrossing in host populations by selecting against selfed offspring, rather than by inducing changes in the propensity to outcross.
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Biparental sex is widespread in nature, yet costly relative to uniparental reproduction. It is generally unclear why self-fertilizing or asexual lineages do not readily invade outcrossing populations. The Red Queen hypothesis predicts that coevolving parasites can prevent self-fertilizing or asexual lineages from invading outcrossing host populations. However, only highly virulent parasites are predicted to maintain outcrossing, which may limit the general applicability of the Red Queen hypothesis. Here, we tested whether the ability of coevolving parasites to prevent invasion of self-fertilization within outcrossing host populations was dependent on parasite virulence. We introduced wild-type Caenorhabditis elegans hermaphrodites, capable of both self-fertilization and outcrossing, into C. elegans populations fixed for a mutant allele conferring obligate outcrossing. Replicate C. elegans populations were exposed for 24 host generations to one of four strains of Serratia marcescens parasites that varied in virulence, under three treatments: a heat-killed (control, noninfectious) parasite treatment, a fixed-genotype (nonevolving) parasite treatment, and a copassaged (potentially coevolving) parasite treatment. As predicted, self-fertilization invaded C. elegans host populations in the control and fixed-parasite treatments, regardless of parasite virulence. In the copassaged treatment, selfing invaded host populations coevolving with low- to mid-virulence strains, but remained rare in hosts coevolving with highly virulent bacterial strains. Therefore, we found that only highly virulent coevolving parasites can impede the invasion of selfing.
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OBJECTIVES: Colloid carcinoma (CC) is a rare subtype of pancreatic carcinoma. The aims of the study are to characterize the clinicopathological features and to evaluate the overall survival (OS) of patients with CC. METHODS: Patients diagnosed with pancreatic CC and pancreatic ductal adenocarcinoma (PDAC) between 2004 and 2016 were identified from the National Cancer Database using International Classification of Disease-O-3 morphology (8480/3 and 8140/3) and topography (C25) codes. Kaplan-Meier analysis and Cox proportional hazards models were used to analyze OS. RESULTS: Fifty-six thousand eight hundred forty-six patients were identified. A total of 2430 patients (4.3%) were diagnosed with pancreatic CC. Males constituted 52.8% of CC and 52.2% of PDAC. Colloid carcinoma presented with pathological stage I disease more often (16.7% vs 5.9%) and stage IV disease less often (42.1% vs 52.4%) than PDAC (P < 0.001). Stage I CC received chemotherapy (36.0% vs 59.4%) and neoadjuvant chemotherapy (4.4% vs 14.2%) less often compared with PDAC (P < 0.001). Statistically significant improved OS was seen among stage I, II, and IV CC compared with PDAC. CONCLUSIONS: Pancreatic CC presented as stage I disease more often compared with PDAC. Neoadjuvant chemotherapy was administered more often in stage I PDAC compared with CC. Colloid carcinoma had improved OS compared with PDAC among all stages except stage III.
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Adenocarcinoma Mucinoso , Carcinoma Ductal Pancreático , Neoplasias Pancreáticas , Masculino , Humanos , Prognóstico , Neoplasias Pancreáticas/diagnóstico , Carcinoma Ductal Pancreático/tratamento farmacológico , Adenocarcinoma Mucinoso/terapia , Adenocarcinoma Mucinoso/patologia , Estudos Retrospectivos , Neoplasias PancreáticasRESUMO
Gene flow into populations can increase additive genetic variation and introduce novel beneficial alleles, thus facilitating adaptation. However, gene flow may also impede adaptation by disrupting beneficial genotypes, introducing deleterious alleles, or creating novel dominant negative interactions. While theory and fieldwork have provided insight into the effects of gene flow, direct experimental tests are rare. Here, we evaluated the effects of gene flow on adaptation in the nematode Caenorhabditis elegans during exposure to the bacterial parasite, Serratia marcescens. We evolved hosts against nonevolving parasites for 10 passages while controlling host gene flow and source population. We used source nematode populations with three different genetic backgrounds (one similar to the sink population and two different) and two evolutionary histories (previously adapted to S. marcescens or naive). We found that populations with gene flow exhibited greater increases in parasite resistance than those without gene flow. Additionally, gene flow from adapted populations resulted in greater increases in resistance than gene flow from naive populations, particularly with gene flow from novel genetic backgrounds. Overall, this work demonstrates that gene flow can facilitate adaptation and suggests that the genetic architecture and evolutionary history of source populations can alter the sink population's response to selection.
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Parasitos , Animais , Fluxo Gênico , Interações Hospedeiro-Patógeno/genética , Serratia marcescens/genética , Adaptação Fisiológica/genética , Caenorhabditis elegans/genética , Interações Hospedeiro-ParasitaRESUMO
Of 65 cases during a human immunodeficiency virus (HIV) outbreak among persons who inject drugs (PWID) in West Virginia (2019-2021), 61 (94%) had hepatitis C diagnosed a median of 46 months prior to HIV diagnosis. Hepatitis C diagnosis among PWID should trigger improved access to prevention and treatment services.
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Usuários de Drogas , Infecções por HIV , Hepatite C , Abuso de Substâncias por Via Intravenosa , Humanos , Hepacivirus , HIV , Abuso de Substâncias por Via Intravenosa/complicações , Abuso de Substâncias por Via Intravenosa/epidemiologia , West Virginia/epidemiologia , Infecções por HIV/complicações , Infecções por HIV/epidemiologia , Infecções por HIV/diagnóstico , Hepatite C/epidemiologia , Surtos de DoençasAssuntos
Usuários de Drogas , Infecções por HIV , Abuso de Substâncias por Via Intravenosa , Humanos , West Virginia/epidemiologia , Surtos de Doenças/prevenção & controle , Infecções por HIV/epidemiologia , Infecções por HIV/prevenção & controle , Abuso de Substâncias por Via Intravenosa/complicações , Abuso de Substâncias por Via Intravenosa/epidemiologiaRESUMO
Differences in diet and lifestyle relative to those of our Paleolithic-era ancestors may explain current high incidences of chronic diseases, including colorectal cancer (CRC), in Westernized countries. Previously reported evolutionary-concordance diet and lifestyle pattern scores, reflecting closeness of diet and lifestyle patterns to those of Paleolithic-era humans, were associated with lower CRC incidence. Separate and joint associations of the scores with colorectal adenoma among men and women are unknown. To address this, we pooled data from three case-control studies of incident, sporadic colorectal adenomas (n = 771 cases, 1,990 controls), used participants' responses to food frequency and lifestyle questionnaires to calculate evolutionary-concordance diet and lifestyle pattern scores, and estimated the scores' associations with adenomas using multivariable unconditional logistic regression. The multivariable-adjusted odds ratios comparing those in the highest relative to the lowest diet and lifestyle score quintiles were 0.84 (95% confidence interval [CI] 0.62, 1.12; Ptrend:0.03) and 0.41 (95% CI 0.29, 0.59; Ptrend:<0.0001), respectively. The inverse associations were stronger for high-risk adenomas, and among those with both high relative to those with both low diet and lifestyle scores. These results suggest that more evolutionary-concordant diet and lifestyle patterns, separately and jointly, may be associated with lower risk for incident, sporadic colorectal adenoma.Supplemental data for this article is available online at https://doi.org/10.1080/01635581.2021.2002919 .
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Adenoma , Neoplasias Colorretais , Adenoma/epidemiologia , Adenoma/etiologia , Estudos de Casos e Controles , Neoplasias Colorretais/epidemiologia , Neoplasias Colorretais/etiologia , Dieta , Feminino , Humanos , Estilo de Vida , Masculino , Fatores de RiscoRESUMO
Host-parasite interactions may often be subject to opposing evolutionary forces, which likely influence the evolutionary trajectories of both partners. Natural selection and genetic drift are two major evolutionary forces that act in host and parasite populations. Further, population size is a significant determinant of the relative strengths of these forces. In small populations, drift may undermine the persistence of beneficial alleles, potentially impeding host adaptation to parasites. Here, we investigate two questions: (a) can selection pressure for increased resistance in small, susceptible host populations overcome the effects of drift and (b) can resistance be maintained in small host populations? To answer these questions, we experimentally evolved the host Caenorhabditis elegans against its bacterial parasite, Serratia marcescens, for 13 host generations. We found that strong selection favouring increased host resistance was insufficient to counteract drift in small populations, resulting in persistently high host mortality. Additionally, in small populations of resistant hosts, we found that selection for the maintenance of resistance is not always sufficient to curb the loss of resistance. We compared these results with selection in large host populations. We found that initially resistant, large host populations were able to maintain high levels of resistance. Likewise, initially susceptible, large host populations were able to gain resistance to the parasite. These results show that strong selection pressure for survival is not always sufficient to counteract drift. In consideration of C. elegans natural population dynamics, we suggest that drift may often impede selection in nature.
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Caenorhabditis elegans/microbiologia , Deriva Genética , Interações Hospedeiro-Parasita/genética , Seleção Genética , Serratia marcescens/fisiologia , Adaptação Biológica , Animais , Evolução Biológica , Caenorhabditis elegans/genética , Caenorhabditis elegans/imunologiaRESUMO
BACKGROUND: Clinico-pathological high-risk features are frequently utilized in adjuvant chemotherapy (AC) decisions in stage II colorectal cancer and their utility in stage II appendiceal adenocarcinoma (AA) is not established. The aim of this study is to determine the impact of high-risk features in clinical outcomes and whether high risk features are predictive of AC benefit in stage II AA. METHODS: Patients with pathological stage II AA between 2010 and 2015 were identified from the National Cancer Database (NCDB) using ICD-O-3 morphology and topography codes: 8140, 8480 and C18.1. High risk stage II AA was defined as having at least one of the following clinicopathological features: T4 tumor, <12 lymph nodes examined, poorly differentiated histology, positive margins, or lymphovascular invasion. Patients with none of these features were defined as low-risk. RESULTS: A total of 1040 patients with pathological stage II AA were identified. 51.0% males, 84.5% Caucasian; median age 61 (range, 19-90). 46.4% were determined to have high-risk stage II AA. High-risk status was associated with worse OS compared to low-risk in univariate (HR 1.55; 95% CI 1.18-2.02; p = 0.001) and multivariable analyses (HR 1.36; 95% CI 1.03-1.79; p = 0.028). High-risk stage II AA patients had significantly worse 5-year OS compared to low-risk patients (67.1% vs. 74.5%, p = 0.0013). AC was administered in 34.4% (n = 166) of high-risk patients and in 36.5% (n = 203) of low-risk patients. Among high-risk patients, AC was not associated with better OS in univariate (HR 0.86; 95% CI 0.59-1.26; p = 0.448) and multivariable analyses (HR 1.35; 95% CI 0.90-2.04; p = 0.151) compared to no AC. Similarly, among low-risk patients, AC was not associated with better OS in univariate (HR 0.92; 95% CI 0.60-1.39; p = 0.679) and multivariable analyses (HR 1.27; 95% CI 0.81-2.02; p = 0.299) compared to no AC. For high-risk patients, 5-year OS was 68.3% in patients that received AC vs. 66.5% in patients that did not (p = 0.722). For low-risk patients, 5-year OS was 74.0% in patients that received AC vs. 76.3% in patients that did not (p = 0.813). CONCLUSION: High-risk stage II AA patients had significantly worse 5-year OS compared to low-risk patients. AC did not improve survival regardless of high-risk features in stage II AA in this retrospective study. A prospective randomized clinical trial would be required to determine the impact of high-risk features on AC in stage II AA.
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Adenocarcinoma/mortalidade , Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico , Neoplasias do Apêndice/mortalidade , Apêndice/patologia , Adenocarcinoma/diagnóstico , Adenocarcinoma/patologia , Adenocarcinoma/terapia , Adulto , Idoso , Idoso de 80 Anos ou mais , Apendicectomia , Neoplasias do Apêndice/diagnóstico , Neoplasias do Apêndice/patologia , Neoplasias do Apêndice/terapia , Apêndice/cirurgia , Quimioterapia Adjuvante/métodos , Quimioterapia Adjuvante/estatística & dados numéricos , Feminino , Humanos , Estimativa de Kaplan-Meier , Masculino , Margens de Excisão , Pessoa de Meia-Idade , Estadiamento de Neoplasias , Estudos Retrospectivos , Medição de Risco/métodos , Fatores de Risco , Adulto JovemRESUMO
OBJECTIVE: Resection of the primary (RP) in metastatic neuroendocrine tumor (NET) is controversial. The aim was to evaluate survival outcomes for RP in metastatic NET patients. METHODS: Data were obtained from US hospitals at the National Cancer Database between 2004 and 2014. χ2, analysis of variance tests, univariate, and multivariate cox proportional hazards models were evaluated. Kaplan-Meier curves and log-rank tests conducted to compare the survival difference of patient characteristics. RESULTS: A total of 2361 patients were identified. The mean age was 62.1 years (standard deviation, 13 years), male-to-female ratio 1:1; 33% were small intestine, 26.3% pancreas, and 24.4% lung; 69.6% were well-differentiated; and 42.5% underwent RP. The 5-year overall survival (OS) was significantly improved for patients who underwent RP in small intestine (5-year OS, 63.9% vs 44.2%), lung (5-year OS, 65.4% vs 20.2%), and pancreas tumors (5-year OS, 75.6% vs 30.6%). On multivariate analysis, RP (hazard ratio, 0.46; 95% confidence interval, 0.29-0.73; P < 0.001), female, year of diagnosis 2010-2014, margin, Charlson-Deyo score less than 2, and age less than 51 years, were associated with better OS. CONCLUSIONS: Resection of the primary in metastatic well-differentiated NET is associated with improved OS compared with no RP.
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Carcinoma Neuroendócrino/cirurgia , Metástase Neoplásica/terapia , Idoso , Feminino , Humanos , Masculino , Margens de Excisão , Pessoa de Meia-Idade , Metástase Neoplásica/fisiopatologia , Modelos de Riscos Proporcionais , Estudos RetrospectivosRESUMO
Theory on the evolution of niche width argues that resource heterogeneity selects for niche breadth. For parasites, this theory predicts that parasite populations will evolve, or maintain, broader host ranges when selected in genetically diverse host populations relative to homogeneous host populations. To test this prediction, we selected the bacterial parasite Serratia marcescens to kill Caenorhabditis elegans in populations that were genetically heterogeneous (50% mix of two experimental genotypes) or homogeneous (100% of either genotype). After 20 rounds of selection, we compared the host range of selected parasites by measuring parasite fitness (i.e. virulence, the selected fitness trait) on the two focal host genotypes and on a novel host genotype. As predicted, heterogeneous host populations selected for parasites with a broader host range: these parasite populations gained or maintained virulence on all host genotypes. This result contrasted with selection in homogeneous populations of one host genotype. Here, host range contracted, with parasite populations gaining virulence on the focal host genotype and losing virulence on the novel host genotype. This pattern was not, however, repeated with selection in homogeneous populations of the second host genotype: these parasite populations did not gain virulence on the focal host genotype, nor did they lose virulence on the novel host genotype. Our results indicate that host heterogeneity can maintain broader host ranges in parasite populations. Individual host genotypes, however, vary in the degree to which they select for specialization in parasite populations.
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Adaptação Biológica , Evolução Biológica , Interações Hospedeiro-Patógeno/genética , Seleção Genética , Serratia marcescens/patogenicidade , Animais , Caenorhabditis elegans , Serratia marcescens/genética , SoftwareRESUMO
Parasites often infect genetically diverse host populations, and the evolutionary trajectories of parasite populations may be shaped by levels of host heterogeneity. Mixed genotype host populations, compared to homogeneous host populations, can reduce parasite prevalence and potentially reduce rates of parasite adaptation due to trade-offs associated with adapting to specific host genotypes. Here, we used experimental evolution to select for increased virulence in populations of the bacterial parasite Serratia marcescens exposed to either heterogeneous or homogeneous populations of Caenorhabditis elegans. We found that parasites exposed to heterogeneous host populations evolved significantly less virulence than parasites exposed to homogeneous host populations over several hundred bacterial generations. Thus, host heterogeneity impeded parasite adaptation to host populations. While we detected trade-offs in virulence evolution, parasite adaptation to two specific host genotypes also resulted in modestly increased virulence against the reciprocal host genotypes. These results suggest that parasite adaptation to heterogeneous host populations may be impeded by both trade-offs and a reduction in the efficacy of selection as different host genotypes exert different selective pressures on a parasite population.
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Evolução Biológica , Parasitos , Adaptação Fisiológica , Animais , Interações Hospedeiro-Parasita , Serratia marcescens , VirulênciaRESUMO
BACKGROUND: Adenocarcinoma (AC) is the most common histological type in gallbladder carcinoma (GBC). Squamous cell carcinoma (SCC), adenosquamous carcinoma (ASC), and papillary carcinoma (PC) are rare histologic variants of GBC. METHODS: Patients with AC, SCC, ASC, and PC of the gallbladder between 2004 and 2013 were identified from the National Cancer Database. Univariate and multivariate analyses were performed, and Kaplan-Meier curves were used to compare overall survival (OS) based on histological subtype. RESULTS: A total of 5956 patients ≥18 years of age were included in the final analysis. Most patients (n = 5398; 90.6%) had AC compared with variant histologies. PC (n = 227; 3.8%) was the most common variant, followed by ASC (n = 216; 3.6%) and SCC (n = 115; 1.9%); 70.3% were female and 78.9% Caucasian. The median age was 70 (range, 25-90) years. Surgical resection was performed in 77.7% of AC, 53.0% of SCC, 88.9% of ASC, and 96.9% of PC (P < .001). Systemic therapy after surgery was administered in 25.1% of AC, 18.3% of SCC, 35.7% of ASC, and 19.4% of PC (P = .001). In multivariate analysis, multiagent chemotherapy was associated with improved OS in all histologies except for SCC and PC (p < .001), and adjuvant systemic therapy was associated with improved OS in ASC and AC (P < .001). CONCLUSION: Survival differs between the gallbladder variants. Except for SCC, GBC variants underwent surgical resection more often than AC. Adjuvant systemic therapy was associated with improved OS in ASC and AC.
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Host-parasite research often focuses on a single host life stage, yet different life stages may exhibit different defenses. The nematode Caenorhabditis elegans has an alternate dispersal life stage, dauer. Despite dauer's importance in nature, we know little of how it responds to parasites. Previous research indicates that non-dauer C. elegans prefer to consume the virulent bacterial parasite, Serratia marcescens, when given a choice between the parasite and benign Escherichia coli. Here, we compared the preferences of dauer individuals from six strains of C. elegans to the preferences of other life stages. We found that dauer individuals exhibited reduced preference for S. marcescens, and dauers from some strains preferred E. coli to S. marcescens. In addition to testing food preference, a mechanism of parasite avoidance, we also measured host mortality rates after direct parasite exposure to determine if life stage also altered host survival. Overall, dauer individuals exhibited reduced mortality rates. However, dauer versus non-dauer larvae mortality rates also varied significantly by host strain. Collectively, we found evidence of dauer-induced parasite avoidance and reduced mortality in the presence of a parasite, but these effects were strain-specific. These results demonstrate the importance of host life stage and genotype when assessing infection dynamics.
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Caenorhabditis elegans/parasitologia , Interações Hospedeiro-Parasita , Serratia marcescens/fisiologia , Animais , Caenorhabditis elegans/crescimento & desenvolvimento , Caenorhabditis elegans/fisiologia , Preferências Alimentares , Estágios do Ciclo de Vida , Infecções por Serratia/fisiopatologia , Infecções por Serratia/veterináriaRESUMO
The yeast Candida albicans is an opportunistic pathogen of humans, meaning that despite commensal interactions with its host, it can transition to a harmful pathogen. While C. albicans is the predominant species isolated in the human gastrointestinal mycobiome and is implicated in fungal infection, infections due to non-albicans Candida species are rapidly rising. Studying the factors that contribute to virulence is often challenging and frequently depends on many contexts, including host immune status and pathogen genetic background. Here, we utilize the nematode Caenorhabditis elegans as a perspicuous and efficient model host system to study fungal infections of Candida pathogens. We find that, in addition to reducing lifetime host survival, exposure to C. albicans results in delayed reproduction, which significantly reduced lineage growth over multiple generations. Furthermore, we assessed fungal pathogen virulence in C. elegans hosts compromised for innate immune function and detected increased early mortality, reduced brood sizes, and delayed reproduction relative to infected healthy hosts. Importantly, by assessing virulence in both healthy and immunocompromised host backgrounds, we reveal the pathogen potential in non-albicans Candida species. Taken together, we present a novel lineage growth assay to measure reduction in host fitness associated with fungal infection and demonstrate significant interactions between pathogen and host immune function that contribute to virulence.IMPORTANCE Opportunistic pathogens are commensals capable of causing disease and are serious threats to human health. It is critical to understand the mechanisms and host contexts under which opportunistic pathogens become virulent. In this work, we present a novel assay to quickly and quantitatively measure pathogen virulence in healthy and immunocompromised nematode hosts. We found that Candida species, one of the most prominent fungal opportunistic pathogens of humans, decrease host fitness by reducing survival and impacting host reproduction. Most importantly, by measuring virulence in hosts that have intact or compromised immune function, we can reveal the pathogenic potential of opportunistic fungal pathogens.
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Caenorhabditis elegans/microbiologia , Candida/patogenicidade , Interações Hospedeiro-Patógeno/imunologia , Hospedeiro Imunocomprometido , Fenótipo , Animais , Caenorhabditis elegans/imunologia , Candidíase/patologia , Proteínas Fúngicas/genética , Imunidade Inata , Reprodução , Análise de Sobrevida , VirulênciaRESUMO
To reveal phenotypic and functional genomic patterns of mitonuclear adaptation, a laboratory adaptation study with Caenorhabditis elegans nematodes was conducted in which independently evolving lines were initiated from a low-fitness mitochondrial electron transport chain (ETC) mutant, gas-1 Following 60 generations of evolution in large population sizes with competition for food resources, two distinct classes of lines representing different degrees of adaptive response emerged: a low-fitness class that exhibited minimal or no improvement compared to the gas-1 mutant ancestor, and a high-fitness class containing lines that exhibited partial recovery of wild-type fitness. Many lines that achieved higher reproductive and competitive fitness levels were also noted to evolve high frequencies of males during the experiment, consistent with adaptation in these lines having been facilitated by outcrossing. Whole-genome sequencing and analysis revealed an enrichment of mutations in loci that occur in a gas-1-centric region of the C. elegans interactome and could be classified into a small number of functional genomic categories. A highly nonrandom pattern of mitochondrial DNA mutation was observed within high-fitness gas-1 lines, with parallel fixations of nonsynonymous base substitutions within genes encoding NADH dehydrogenase subunits I and VI. These mitochondrial gene products reside within ETC complex I alongside the nuclear-encoded GAS-1 protein, suggesting that rapid adaptation of select gas-1 recovery lines was driven by fixation of compensatory mitochondrial mutations.
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Adaptação Fisiológica , Caenorhabditis elegans/genética , DNA Mitocondrial/genética , Evolução Molecular , Razão de Masculinidade , Animais , Caenorhabditis elegans/fisiologia , Proteínas de Caenorhabditis elegans/genética , Epistasia Genética , Frequência do Gene , Aptidão Genética , Hibridização Genética , Masculino , NADH Desidrogenase/genéticaRESUMO
Host susceptibility to parasites can vary over space and time. Costs associated with the maintenance of host defence are thought to account for a portion of this variation. Specifically, trade-offs wherein elevated defence is maintained at the cost of fitness in the absence of the parasite may cause levels of host defence to change over time and differ between populations. In previous studies, we found that populations of the host nematode, Caenorhabditis elegans, evolved greater levels of parasite avoidance and resistance against the bacterial parasite, Serratia marcescens. Here, we passaged these host populations either in the presence or absence of the parasite to test for a cost of elevated host defences. After 16 generations, we found that elevated levels of host defence were maintained during evolution in both the presence and absence of the parasite. Further, this maintenance of defence was not the result of limited standing genetic variation, but rather the absence of a measurable cost associated with defence. Therefore, costs associated with host defence may not broadly account for differences in host susceptibility across space and time.
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Caenorhabditis elegans/genética , Caenorhabditis elegans/microbiologia , Aptidão Genética , Serratia/fisiologia , Animais , Evolução Biológica , Interações Hospedeiro-Patógeno/genética , Interações Hospedeiro-Patógeno/imunologiaRESUMO
The ubiquity of outcrossing in plants and animals is difficult to explain given its costs relative to self-fertilization. Despite these costs, exposure to changing environmental conditions can temporarily favor outcrossing over selfing. Therefore, recurring episodes of environmental change are predicted to favor the maintenance of outcrossing. Studies of host-parasite coevolution have provided strong support for this hypothesis. However, it is unclear whether multiple exposures to novel parasite genotypes in the absence of coevolution are sufficient to favor outcrossing. Using the nematode Caenorhabditis elegans and the bacterial parasite Serratia marcescens, we studied host responses to parasite turnover. We passaged several replicates of a host population that was well-adapted to the S. marcescens strain Sm2170 with either Sm2170 or one of three novel S. marcescens strains, each derived from Sm2170, for 18 generations. We found that hosts exposed to novel parasites maintained higher outcrossing rates than hosts exposed to Sm2170. Nonetheless, host outcrossing rates declined over time against all but the most virulent novel parasite strain. Hosts exposed to the most virulent novel strain exhibited increased outcrossing rates for approximately 12 generations, but did not maintain elevated levels of outcrossing throughout the experiment. Thus, parasite turnover can transiently increase host outcrossing. These results suggest that recurring episodes of parasite turnover have the potential to favor the maintenance of host outcrossing. However, such maintenance may require frequent exposure to novel virulent parasites, rapid rates of parasite turnover, and substantial host gene flow.
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Accurate measurements of an organism's fitness are crucial for measuring evolutionary change. Methods of fitness measurement are most accurate when incorporating an individual's survival and fecundity, as well as accounting for any ecological interactions or environmental effects experienced by the organism. Here, we describe a protocol for measuring the relative mean fitness of Caenorhabditis elegans populations, or strains, through an assay that accounts for individual survival, fecundity, and intraspecific competitive ability in the presence of a bacterial parasite. In this competitive fitness assay nematodes from a focal population or strain are mixed with a GFP-marked tester strain in equal proportions, the mixture of nematodes are then exposed to a parasite, and the relative competitive fitness of the focal strain is determined by measuring the change in the ratio of focal nematodes to GFP-marked nematodes after one generation. Specifically, this protocol can be implemented to measure changes in nematode host fitness after experimental evolution by determining the relative competitive fitness of evolved versus ancestral nematode populations.
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Hosts exhibit a variety of defence mechanisms against parasites, including avoidance. Both host-parasite coevolutionary dynamics and the host mating system can alter the evolutionary trajectories of populations. Does the nature of host-parasite interactions and the host mating system affect the mechanisms that evolve to confer host defence? In a previous experimental evolution study, mixed mating and obligately outcrossing Caenorhabditis elegans host populations adapted to either coevolving or static Serratia marcescens parasite populations. Here, we assessed parasite avoidance as a mechanism underlying host adaptation. We measured host feeding preference for the coevolved and static parasites vs preference for Escherichia coli, to assess the evolution of avoidance behaviour within our experiment. We found that mixed mating host populations evolved a preference for E. coli relative to the static parasite strain; therefore, the hosts evolved parasite avoidance as a defence. However, mixed mating hosts did not exhibit E. coli preference when exposed to coevolved parasites, so avoidance cannot account for host adaptation to coevolving parasites. Further, the obligately outcrossing host populations did not exhibit parasite avoidance in the presence of either static or coevolved parasites. Therefore, both the nature of host-parasite interactions and the host mating system shaped the evolution of host defence.