scholarly journals Host heterogeneity mitigates virulence evolution

2020 ◽  
Vol 16 (1) ◽  
pp. 20190744 ◽  
Author(s):  
P. Signe White ◽  
Angela Choi ◽  
Rishika Pandey ◽  
Arthur Menezes ◽  
McKenna Penley ◽  
...  
Keyword(s):  
Experimental Evolution ◽  
Parasite Prevalence ◽  
Mixed Genotype ◽  
Selective Pressures ◽  
Virulence Evolution ◽  
Specific Host ◽  
Trade Offs ◽  
Evolutionary Trajectories ◽  
Parasite Populations ◽  
Host Heterogeneity

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.

scholarly journals How to maintain a high virulence: evolution of a killer in hosts of various susceptibilities

2019 ◽  
Author(s):  
Aurélien Chateigner ◽  
Yannis Moreau ◽  
Davy Jiolle ◽  
Cindy Pontlevé ◽  
Carole Labrousse ◽  
...  
Keyword(s):  
Experimental Evolution ◽  
Transmission Probability ◽  
Evolutionary Potential ◽  
Virulence Evolution ◽  
Specific Host ◽  
Trade Offs ◽  
Virulent Strains ◽  
High Virulence ◽  
Infection Cycles ◽  
Highly Virulent

AbstractPathogens should evolve to avirulence. However, while baculoviruses can be transmitted through direct contact, their main route of infection goes through the death and liquefaction of their caterpillar hosts and highly virulent strains still seem to be advantaged through infection cycles. Furthermore, one of them,Autographa californicamultiple nucleopolyhedrovirus, is so generalist that it can infect more than 100 different hosts.To understand and characterize the evolutionary potential of this virus and how it is maintained while killing some of its hosts in less than a week, we performed an experimental evolution starting from an almost natural isolate of AcMNPV, known for its generalist infection capacity. We made it evolve on 4 hosts of different susceptibilities for 10 cycles and followed hosts survival each day. We finally evaluated whether the generalist capacity was maintained after evolving on one specific host species and tested an epidemiological model through simulations to understand how.Finally, on very highly susceptible hosts, transmission-virulence trade-offs seem to disappear and the virus can maximize transmission and virulence. When less adapted to its host, the pathogen’s virulence has not been modified along cycles but the yield was increased, apparently through an increased transmission probability and an increased latent period between exposition and infection.

Single-clone and mixed-clone infections versus host environment in Crithidia bombi infecting bumblebees

Parasitology ◽  
1998 ◽  
Vol 117 (4) ◽  
pp. 331-336 ◽  
Author(s):  
B. IMHOOF ◽  
P. SCHMID-HEMPEL
Keyword(s):  
Bombus Terrestris ◽  
Infection Intensity ◽  
Parasite Prevalence ◽  
Mixed Genotype ◽  
Host Environment ◽  
Crithidia Bombi ◽  
The Family ◽  
Single Clone ◽  
Parasite Evolution ◽  
Host Heterogeneity

Current theories assume that adaptive parasite evolution explains variation in the level of virulence and parasite success. In particular, mixed-genotype infections by parasites should generally be more virulent, and faster multiplying strains more successful, either because fixed strategies have evolved or because parasites facultatively alter virulence in response to co-infecting competitors. We compared several measures of parasite success and virulence between single-clone and mixed-clone infections of 2 strains of the trypanosome Crithidia bombi in its bumblebee host, Bombus terrestris. Contrary to expectation, we could not find differences between single-clone and mixed-clone infections in parasite prevalence, infection success, duration and clearance rate. However, a clearly significant effect of colony on infection intensity was present, and the colony effect emerged in virtually all other measures. We thus conclude that host environment as defined by the family (colony) genotype and thus host heterogeneity are more important in determining parasite virulence than the parasite characteristics. This does not invalidate modern theories of parasite evolution but suggests that variation in both hosts and parasites must be taken into account in more detail.

scholarly journals Sexual conflict drives micro- and macroevolution of sexual dimorphism in immunity

BMC Biology ◽  
2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Basabi Bagchi ◽  
Quentin Corbel ◽  
Imroze Khan ◽  
Ellen Payne ◽  
Devshuvam Banerji ◽  
...  
Keyword(s):  
Sex Differences ◽  
Sexual Dimorphism ◽  
Mating System ◽  
Sexual Conflict ◽  
Experimental Evolution ◽  
Parasitic Infections ◽  
Pathogen Dynamics ◽  
Trade Offs ◽  
Host Pathogen ◽  
Seed Beetles

Abstract Background Sexual dimorphism in immunity is believed to reflect sex differences in reproductive strategies and trade-offs between competing life history demands. Sexual selection can have major effects on mating rates and sex-specific costs of mating and may thereby influence sex differences in immunity as well as associated host–pathogen dynamics. Yet, experimental evidence linking the mating system to evolved sexual dimorphism in immunity are scarce and the direct effects of mating rate on immunity are not well established. Here, we use transcriptomic analyses, experimental evolution and phylogenetic comparative methods to study the association between the mating system and sexual dimorphism in immunity in seed beetles, where mating causes internal injuries in females. Results We demonstrate that female phenoloxidase (PO) activity, involved in wound healing and defence against parasitic infections, is elevated relative to males. This difference is accompanied by concomitant sex differences in the expression of genes in the prophenoloxidase activating cascade. We document substantial phenotypic plasticity in female PO activity in response to mating and show that experimental evolution under enforced monogamy (resulting in low remating rates and reduced sexual conflict relative to natural polygamy) rapidly decreases female (but not male) PO activity. Moreover, monogamous females had evolved increased tolerance to bacterial infection unrelated to mating, implying that female responses to costly mating may trade off with other aspects of immune defence, an hypothesis which broadly accords with the documented sex differences in gene expression. Finally, female (but not male) PO activity shows correlated evolution with the perceived harmfulness of male genitalia across 12 species of seed beetles, suggesting that sexual conflict has a significant influence on sexual dimorphisms in immunity in this group of insects. Conclusions Our study provides insights into the links between sexual conflict and sexual dimorphism in immunity and suggests that selection pressures moulded by mating interactions can lead to a sex-specific mosaic of immune responses with important implications for host–pathogen dynamics in sexually reproducing organisms.

scholarly journals Chance, contingency, and necessity in the experimental evolution of ancestral proteins

2020 ◽  
Author(s):  
Victoria Cochran Xie ◽  
Jinyue Pu ◽  
Brian P.H. Metzger ◽  
Joseph W. Thornton ◽  
Bryan C. Dickinson
Keyword(s):  
Protein Evolution ◽  
Experimental Evolution ◽  
Cell Lymphoma ◽  
B Cell Lymphoma ◽  
Sequence Evolution ◽  
Protein Protein Interaction ◽  
Evolutionary Trajectories ◽  
Historical Moment ◽  
Related Proteins ◽  
Ancestral Protein

SUMMARYThe extent to which chance and contingency shaped the sequence outcomes of protein evolution is largely unknown. To directly characterize the causes and consequences of chance and contingency, we combined directed evolution with ancestral protein reconstruction. By repeatedly selecting a phylogenetic series of ancestral proteins in the B-cell lymphoma-2 family to evolve the same protein-protein interaction specificities that existed during history, we show that contingency and chance interact to make sequence evolution almost entirely unpredictable over the timescale of metazoan evolution. At any historical moment, multiple sets of mutations can alter or maintain specificity, and chance decides which ones occur. Contingency arises because historical sequence substitutions epistatically altered which mutations are compatible with new or ancestral functions. Evolutionary trajectories launched from different ancestors therefore lead to dramatically different outcomes over phylogenetic time, with virtually no mutations occurring repeatedly in distantly related proteins, even under identical selection conditions.

scholarly journals Vertebrate cardiac regeneration: evolutionary and developmental perspectives

2021 ◽  
Vol 10 (1) ◽  
Author(s):  
Stephen Cutie ◽  
Guo N. Huang
Keyword(s):  
Cardiac Injury ◽  
Adaptive Immune System ◽  
Cardiac Regeneration ◽  
Heart Regeneration ◽  
Adaptive Immune ◽  
Selective Pressures ◽  
Trade Offs ◽  
Lower Vertebrates ◽  
Complex Adaptive ◽  
And Function

AbstractCardiac regeneration is an ancestral trait in vertebrates that is lost both as more recent vertebrate lineages evolved to adapt to new environments and selective pressures, and as members of certain species developmentally progress towards their adult forms. While higher vertebrates like humans and rodents resolve cardiac injury with permanent fibrosis and loss of cardiac output as adults, neonates of these same species can fully regenerate heart structure and function after injury – as can adult lower vertebrates like many teleost fish and urodele amphibians. Recent research has elucidated several broad factors hypothesized to contribute to this loss of cardiac regenerative potential both evolutionarily and developmentally: an oxygen-rich environment, vertebrate thermogenesis, a complex adaptive immune system, and cancer risk trade-offs. In this review, we discuss the evidence for these hypotheses as well as the cellular participators and molecular regulators by which they act to govern heart regeneration in vertebrates.

scholarly journals Contingent evolution of alternative metabolic network topologies determines whether cross-feeding evolves

2020 ◽  
Vol 3 (1) ◽  
Author(s):  
Jeroen Meijer ◽  
Bram van Dijk ◽  
Paulien Hogeweg
Keyword(s):  
Metabolic Networks ◽  
Mechanistic Model ◽  
Building Blocks ◽  
Division Of Labour ◽  
Ecosystem Structure ◽  
Evolutionary Contingency ◽  
Trade Offs ◽  
Evolutionary Trajectories ◽  
Network Topologies ◽  
Metabolic Strategies

AbstractMetabolic exchange is widespread in natural microbial communities and an important driver of ecosystem structure and diversity, yet it remains unclear what determines whether microbes evolve division of labor or maintain metabolic autonomy. Here we use a mechanistic model to study how metabolic strategies evolve in a constant, one resource environment, when metabolic networks are allowed to freely evolve. We find that initially identical ancestral communities of digital organisms follow different evolutionary trajectories, as some communities become dominated by a single, autonomous lineage, while others are formed by stably coexisting lineages that cross-feed on essential building blocks. Our results show how without presupposed cellular trade-offs or external drivers such as temporal niches, diverse metabolic strategies spontaneously emerge from the interplay between ecology, spatial structure, and metabolic constraints that arise during the evolution of metabolic networks. Thus, in the long term, whether microbes remain autonomous or evolve metabolic division of labour is an evolutionary contingency.

scholarly journals Experimental Evolution In Vivo To Identify Selective Pressures during Pneumococcal Colonization

mSystems ◽  
2020 ◽  
Vol 5 (3) ◽  
Author(s):  
Vaughn S. Cooper ◽  
Erin Honsa ◽  
Hannah Rowe ◽  
Christopher Deitrick ◽  
Amy R. Iverson ◽  
...  
Keyword(s):  
Streptococcus Pneumoniae ◽  
Murine Model ◽  
Experimental Evolution ◽  
Nasal Colonization ◽  
Content Type ◽  
Selective Pressures ◽  
Specific Tissue ◽  
Tissue Tropisms ◽  
Insight Into

ABSTRACT Experimental evolution is a powerful technique to understand how populations evolve from selective pressures imparted by the surrounding environment. With the advancement of whole-population genomic sequencing, it is possible to identify and track multiple contending genotypes associated with adaptations to specific selective pressures. This approach has been used repeatedly with model species in vitro, but only rarely in vivo. Herein we report results of replicate experimentally evolved populations of Streptococcus pneumoniae propagated by repeated murine nasal colonization with the aim of identifying gene products under strong selection as well as the population genetic dynamics of infection cycles. Frameshift mutations in one gene, dltB, responsible for incorporation of d-alanine into teichoic acids on the bacterial surface, evolved repeatedly and swept to high frequency. Targeted deletions of dltB produced a fitness advantage during initial nasal colonization coupled with a corresponding fitness disadvantage in the lungs during pulmonary infection. The underlying mechanism behind the fitness trade-off between these two niches was found to be enhanced adherence to respiratory cells balanced by increased sensitivity to host-derived antimicrobial peptides, a finding recapitulated in the murine model. Additional mutations that are predicted to affect trace metal transport, central metabolism, and regulation of biofilm production and competence were also selected. These data indicate that experimental evolution can be applied to murine models of pathogenesis to gain insight into organism-specific tissue tropisms. IMPORTANCE Evolution is a powerful force that can be experimentally harnessed to gain insight into how populations evolve in response to selective pressures. Herein we tested the applicability of experimental evolutionary approaches to gain insight into how the major human pathogen Streptococcus pneumoniae responds to repeated colonization events using a murine model. These studies revealed the population dynamics of repeated colonization events and demonstrated that in vivo experimental evolution resulted in highly reproducible trajectories that reflect the environmental niche encountered during nasal colonization. Mutations impacting the surface charge of the bacteria were repeatedly selected during colonization and provided a fitness benefit in this niche that was counterbalanced by a corresponding fitness defect during lung infection. These data indicate that experimental evolution can be applied to models of pathogenesis to gain insight into organism-specific tissue tropisms.

scholarly journals Sexual Size Dimorphism and Morphological Evidence Supporting the Recognition of two Subspecies in the Galápagos Dove

The Condor ◽  
2007 ◽  
Vol 109 (1) ◽  
pp. 132-141
Author(s):  
Diego Santiago-Alarcon ◽  
Patricia G. Parker
Keyword(s):  
Body Size ◽  
Sexual Size Dimorphism ◽  
Bird Species ◽  
Morphological Data ◽  
Morphological Evidence ◽  
Life History Variation ◽  
Size Dimorphism ◽  
Selective Pressures ◽  
Trade Offs ◽  
Discriminant Analyses

Abstract Abstract Sexual size dimorphism is a conspicuous trait of many wild bird species. Differences in body size between the sexes might reflect selective pressures and trade-offs to optimize performance. Here, we analyze the size dimorphism of the Galápagos Dove (Zenaida galapagoensis) using principal component and discriminant analyses with samples obtained from six islands: Santiago, Santa Fe, Santa Cruz, Española, Genovesa, and Wolf. We also reanalyze published morphological data but also including additional samples from Wolf Island to account for morphological differences among islands. Males were significantly larger than females. Discriminant analyses correctly classified 98% of males and 100% of females, and cross-validation of the model correctly classified 97% of males and 98% of females. We created two sexual size dimorphism indices using wing chord and tarsus as body-size surrogates. Significant differences were found in the sexual size dimorphism index for both measurements among islands. Significant differences in sexual size dimorphism among islands might indicate the role of different selective pressures acting on individual islands (e.g., competition, predation, resources, sexual selection), which might result in life history variation of the species among islands. For the first time, we provide significant morphological evidence supporting the classification of the Galápagos Dove into two subspecies: Z. g. galapagoensis and Z. g. exsul.

scholarly journals Phenotypic plasticity and diversity in insects

2010 ◽  
Vol 365 (1540) ◽  
pp. 593-603 ◽  
Author(s):  
Armin P. Moczek
Keyword(s):  
Gene Expression ◽  
Phenotypic Plasticity ◽  
Natural Populations ◽  
Evolutionary Developmental Biology ◽  
Life Cycles ◽  
Biological Organization ◽  
Trade Off ◽  
Evolutionary Innovation ◽  
Trade Offs ◽  
Evolutionary Trajectories

Phenotypic plasticity in general and polyphenic development in particular are thought to play important roles in organismal diversification and evolutionary innovation. Focusing on the evolutionary developmental biology of insects, and specifically that of horned beetles, I explore the avenues by which phenotypic plasticity and polyphenic development have mediated the origins of novelty and diversity. Specifically, I argue that phenotypic plasticity generates novel targets for evolutionary processes to act on, as well as brings about trade-offs during development and evolution, thereby diversifying evolutionary trajectories available to natural populations. Lastly, I examine the notion that in those cases in which phenotypic plasticity is underlain by modularity in gene expression, it results in a fundamental trade-off between degree of plasticity and mutation accumulation. On one hand, this trade-off limits the extent of plasticity that can be accommodated by modularity of gene expression. On the other hand, it causes genes whose expression is specific to rare environments to accumulate greater variation within species, providing the opportunity for faster divergence and diversification between species, compared with genes expressed across environments. Phenotypic plasticity therefore contributes to organismal diversification on a variety of levels of biological organization, thereby facilitating the evolution of novel traits, new species and complex life cycles.

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