Recognition and polymorphism in host—parasite genetics

1994 ◽  
Vol 346 (1317) ◽  
pp. 283-293 ◽  
Keyword(s):  
Host Resistance ◽  
Restriction Enzymes ◽  
Toxin Production ◽  
Dynamical Analysis ◽  
Low Frequencies ◽  
True Nature ◽  
Evolutionary Force ◽  
Recognition Systems ◽  
Plant Pathogen Interactions ◽  
Host Parasite

Genetic specificity occurs in many host-parasite systems. Each host can recognize and resist only a subset of parasites; each parasite can grow only on particular hosts. Biochemical recognition systems determine which matching host and parasite genotypes result in resistance or disease. Recognition systems are often associated with widespread genetic polymorphism in the host and parasite populations. I describe four systems with matching host—parasite polymorphisms: plant-pathogen interactions, nuclear—cytoplasmic conflict in plants, restriction enzymes in bacterial defence against viruses, and bacterial plasmids that compete by toxin production and toxin immunity. These systems highlight several inductive problems. For example, the observed patterns of resistance and susceptibility between samples of hosts and parasites are often used to study polymorphism. The detectable polymorphism by this method may be a poor guide to the actual polymorphism and to the underlying biochemistry of host-parasite recognition. The problem of using detectable polymorphism to infer the true nature of recognition and polymorphism is exacerbated by non-equilibrium fluctuations in allele frequencies that commonly occur in host-parasite systems. Another problem is that different matching systems may lead either to low frequencies of host resistance and common parasites, or to common resistance and rare parasites. Thus low levels of host resistance or rare parasites do not imply that parasitism is an unimportant evolutionary force on host diversity. Knowledge of biochemical recognition systems and dynamical analysis of models provide a framework for analysing the widespread polymorphisms in host-parasite genetics.

scholarly journals Draft Genome Sequence of Plasmopara viticola , the Grapevine Downy Mildew Pathogen

2016 ◽  
Vol 4 (5) ◽  
Author(s):  
Yann Dussert ◽  
Jérôme Gouzy ◽  
Sylvie Richart-Cervera ◽  
Isabelle D. Mazet ◽  
Laurent Delière ◽  
...  
Keyword(s):  
Downy Mildew ◽  
Genome Sequence ◽  
Genome Analysis ◽  
Plant Pathogen ◽  
Host Resistance ◽  
Draft Genome ◽  
Plasmopara Viticola ◽  
Host Specialization ◽  
Grapevine Downy Mildew ◽  
Plant Pathogen Interactions

Plasmopara viticola is a biotrophic pathogenic oomycete responsible for grapevine downy mildew. We present here the first draft of the P. viticola genome. Analysis of this sequence will help in understanding plant-pathogen interactions in oomycetes, especially pathogen host specialization and adaptation to host resistance.

scholarly journals Crystal Toxins and the volunteer’s dilemma in bacteria

2018 ◽  
Keyword(s):  
Genetic Relatedness ◽  
Toxin Production ◽  
Bacterial Cells ◽  
Low Frequencies ◽  
The Public ◽  
Volunteer’S Dilemma ◽  
Cry Toxin ◽  
The Social ◽  
Selection For ◽  
Crystal Toxins

1AbstractThe growth and virulence of the bacteriaBacillus thuringiensisdepends on the production of Cry toxins, which are used to perforate the gut of its host. Successful invasion of the host relies on producing a threshold amount of toxin, after which there is no benefit from producing more toxin. Consequently, the production of Cry toxin appears to be a different type of social problem compared with the public goods scenarios that bacteria often encounter. We show that selection for toxin production is a volunteer’s dilemma. We make the specific predictions that: (1) selection for toxin production depends upon an interplay between the number of bacterial cells that each host ingests, and the genetic relatedness between those cells; (2) cheats that do not produce toxin gain an advantage when at low frequencies, and at high bacterial density, allowing them to be maintained in a population alongside toxin producing cells. More generally, our results emphasise the diversity of the social games that bacteria play.

scholarly journals A test of the Baldwin Effect: Differences in both constitutive expression and inducible responses to parasites underlie variation in host response to a parasite

2020 ◽  
Author(s):  
Lauren Fuess ◽  
Jesse N. Weber ◽  
Stijn den Haan ◽  
Natalie C. Steinel ◽  
Kum Chuan Shim ◽  
...  
Keyword(s):  
Gene Expression ◽  
Host Resistance ◽  
Gasterosteus Aculeatus ◽  
Constitutive Expression ◽  
Baldwin Effect ◽  
Data Set ◽  
Host Parasite Interactions ◽  
Evolution Of Resistance ◽  
Host Parasite ◽  
The Baldwin Effect

ABSTRACTDespite the significant effect of host-parasite interactions on both ecological systems and organism health, there is still limited understanding of the mechanisms driving evolution of host resistance to parasites. One model of rapid evolution, the Baldwin Effect, describes the role of plasticity in adaptation to novel conditions, and subsequent canalization of associated traits. While mostly applied in the context of environmental conditions, this theory may be relevant to the evolution of host resistance to novel parasites. Here we test the applicability of the Baldwin Effect to the evolution of resistance in a natural system using threespine stickleback fish (Gasterosteus aculeatus) and their cestode parasite Schistochephalus solidus. We leverage a large transcriptomic data set to describe the response to S. solidus infection by three different genetic crosses of stickleback, from a resistant and a tolerant population. Hosts mount a multigenic response to the parasite that is similar among host genotypes. In addition, we document extensive constitutive variation in gene expression among host genotypes. However, although many genes are both infection-induced and differentially expressed between genotypes, this overlap is not more extensive than expected by chance. We also see little evidence of canalization of infection-induced gene expression in the derived resistant population. These patterns do not support the Baldwin Effect, though they illustrate the importance of variation in both constitutive expression and induced responses to parasites. Finally, our results improve understanding of the cellular mechanisms underlying a putative resistance phenotype (fibrosis). Combined, our results highlight the importance of both constitutive and inducible variation in the evolution of resistance to parasites, and identify new target genes contributing to fibrosis. These findings advance understanding of host-parasite interactions and co-evolutionary relationships in natural systems.

scholarly journals An alternative route of bacterial infection associated with a novel resistance locus in the Daphnia–Pasteuria host–parasite system

Heredity ◽  
2020 ◽  
Vol 125 (4) ◽  
pp. 173-183
Author(s):  
Gilberto Bento ◽  
Peter D. Fields ◽  
David Duneau ◽  
Dieter Ebert
Keyword(s):  
Host Resistance ◽  
Natural Populations ◽  
Attachment Site ◽  
Genomic Region ◽  
Infection Process ◽  
Resistance Locus ◽  
Significant Qtls ◽  
Novel Host ◽  
Trait Locus ◽  
Host Parasite

Abstract To understand the mechanisms of antagonistic coevolution, it is crucial to identify the genetics of parasite resistance. In the Daphnia magna–Pasteuria ramosa host–parasite system, the most important step of the infection process is the one in which P. ramosa spores attach to the host’s foregut. A matching-allele model (MAM) describes the host–parasite genetic interactions underlying attachment success. Here we describe a new P. ramosa genotype, P15, which, unlike previously studied genotypes, attaches to the host’s hindgut, not to its foregut. Host resistance to P15 attachment shows great diversity across natural populations. In contrast to P. ramosa genotypes that use foregut attachment, P15 shows some quantitative variation in attachment success and does not always lead to successful infections, suggesting that hindgut attachment represents a less-efficient infection mechanism than foregut attachment. Using a Quantitative Trait Locus (QTL) approach, we detect two significant QTLs in the host genome: one that co-localizes with the previously described D. magna PR locus of resistance to foregut attachment, and a second, major QTL located in an unlinked genomic region. We find no evidence of epistasis. Fine mapping reveals a genomic region, the D locus, of ~13 kb. The discovery of a second P. ramosa attachment site and of a novel host-resistance locus increases the complexity of this system, with implications for both for the coevolutionary dynamics (e.g., Red Queen and the role of recombination), and for the evolution and epidemiology of the infection process.

Host Resistance in a Natural Host-Parasite System. Resistance to Hymenolepis citelli by Peromyscus maniculatus

1973 ◽  
Vol 59 (1) ◽  
pp. 117 ◽  
Author(s):  
Donald L. Wassom ◽  
Vance M. Guss ◽  
Albert W. Grundmann
Keyword(s):  
Host Resistance ◽  
Peromyscus Maniculatus ◽  
Natural Host ◽  
Host Parasite

scholarly journals Parasite Microbiome Project: Systematic Investigation of Microbiome Dynamics within and across Parasite-Host Interactions

mSystems ◽  
2017 ◽  
Vol 2 (4) ◽  
Author(s):  
Nolwenn M. Dheilly ◽  
Daniel Bolnick ◽  
Seth Bordenstein ◽  
Paul J. Brindley ◽  
Cédric Figuères ◽  
...  
Keyword(s):  
Host Resistance ◽  
Systematic Investigation ◽  
Model Systems ◽  
Collaborative Effort ◽  
Host Interactions ◽  
Associated Diseases ◽  
Host Parasite Interactions ◽  
Experimental Approaches ◽  
Host Parasite

ABSTRACT Understanding how microbiomes affect host resistance, parasite virulence, and parasite-associated diseases requires a collaborative effort between parasitologists, microbial ecologists, virologists, and immunologists. We hereby propose the Parasite Microbiome Project to bring together researchers with complementary expertise and to study the role of microbes in host-parasite interactions. Understanding how microbiomes affect host resistance, parasite virulence, and parasite-associated diseases requires a collaborative effort between parasitologists, microbial ecologists, virologists, and immunologists. We hereby propose the Parasite Microbiome Project to bring together researchers with complementary expertise and to study the role of microbes in host-parasite interactions. Data from the Parasite Microbiome Project will help identify the mechanisms driving microbiome variation in parasites and infected hosts and how that variation is associated with the ecology and evolution of parasites and their disease outcomes. This is a call to arms to prevent fragmented research endeavors, encourage best practices in experimental approaches, and allow reliable comparative analyses across model systems. It is also an invitation to foundations and national funding agencies to propel the field of parasitology into the microbiome/metagenomic era.

Eimeria nieschulzi infections in inbred and outbred rats: infective dose, route of infection, and host resistance

1973 ◽  
Vol 51 (2) ◽  
pp. 273-279 ◽  
Author(s):  
Eugene M. Liburd
Keyword(s):  
Host Resistance ◽  
Reproductive Potential ◽  
Total Resistance ◽  
Route Of Infection ◽  
Inbred Rats ◽  
Infective Dose ◽  
Eimeria Nieschulzi ◽  
Host Parasite ◽  
Dose Dependent ◽  
Mechanical Crushing

Some of the host–parasite interrelationships between Eimeria nieschulzi (Protozoa: Sporozoa) and inbred and outbred strains of rats, were analyzed. The sex of the host did not influence the severity of infection; however, starved rats as compared with fed ones produced significantly lower numbers of oocysts during an infection. Mechanical crushing of infected faeces yielded a significantly higher number of oocysts than those crushed manually. The reproductive potential of the parasite varied inversely with the dosage of oocysts. Infections were caused by parenteral injections of sporozoites through four routes. In every case these inoculations caused milder infections than those elicited by similar doses of oocysts or sporozoites given orally. All infections stimulated resistance in rats; the intensity of this immunity was dose dependent. Single doses of 2500 and 3500 oocysts or more induced total resistance in outbred and inbred rats, respectively. This immunity was demonstrated 15 days after inoculation, by challenge infections. No developing stages were found in the intestinal tissues of rats which were immunized and then challenged.

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