scholarly journals Population Genetics of Fungal and Oomycete Effectors Involved in Gene-for-Gene Interactions

2009 ◽  
Vol 22 (4) ◽  
pp. 371-380 ◽  
Author(s):  
Eva H. Stukenbrock ◽  
Bruce A. McDonald

Antagonistic coevolution between plants and pathogens has generated a broad array of attack and defense mechanisms. In the classical avirulence (Avr) gene-for-gene model, the pathogen gene evolves to escape host recognition while the host resistance (R) gene evolves to track the evolving pathogen elicitor. In the case of host-specific toxins (HST), the evolutionary arms race may be inverted, with the gene encoding the pathogen toxin evolving to maintain recognition of the host sensitivity target while the host sensitivity gene evolves to escape binding with the toxin. Pathogen effector genes, including those encoding Avr elicitors and HST, often show elevated levels of polymorphism reflecting the coevolutionary arms race between host and pathogen. However, selection can also eliminate variation in the coevolved gene and its neighboring regions when advantageous alleles are swept to fixation. The distribution and diversity of corresponding host genes will have a major impact on the distribution and diversity of effectors in the pathogen population. Population genetic analyses including both hosts and their pathogens provide an essential tool to understand the diversity and dynamics of effector genes. Here, we summarize current knowledge about the population genetics of fungal and oomycete effector genes, focusing on recent studies that have used both spatial and temporal collections to assess the diversity and distribution of alleles and to monitor changes in allele frequencies over time. These studies illustrate that effector genes exhibit a significant degree of diversity at both small and large sampling scales, suggesting that local selection plays an important role in their evolution. They also illustrate that Avr elicitors and HST may be recognizing the same R genes in plants, leading to evolutionary outcomes that differ for necrotrophs and biotrophs while affecting the evolution of the corresponding R genes. Under this scenario, the optimal number of R genes in a plant genome may be determined by the relative abundance of necrotrophic and biotrophic pathogens in the plant's environment.

1989 ◽  
Vol 37 (3) ◽  
pp. 161 ◽  
Author(s):  
WB Sherwin ◽  
ND Murray

This article summarises current knowledge of marsupial population genetics, and discusses its relevance to the conservation of marsupial species. It has been suggested that there is much lower genetic variation within marsupial populations than in eutherian mammals. This trend is not evident in the electrophoretic data summarised here. However, genetic differentiation between populations, subspecies, and species of marsupials appears to be slightly lower than comparable values for eutherians. Genetic estimates of migration between populations are scarce at present, but show values that are comparable with eutherians. Some studies of marsupial population genetics have used non-electrophoretic characteristics, or have addressed the possibility of selection on the characters analysed. Although few, these studies indicate the suitability of marsupials for such investigations. Recent debate over the theories and applications of conservation genetics has made it clear that more research is required on individual species. Given the record of extinction of marsupials in the last 200 years, it is important to test the applicability of these theories to individual marsupial species. Several examples are discussed emphasising the need for ecological studies that estimate the effective number of reproducing individuals per generation. This figure, called the effective size, is the corner- stone of conservation genetics theory, being an important determinant of both the rate of loss of variation between individuals, and the rate of inbreeding. The effective size of the mainland population of the eastern barred bandicoot, Perameles gunnii, appears to be only about one-tenth of its census number. This result is comparable with estimates made in other vertebrates, and demonstrates that many marsupial species which appear to have an adequate census size on ecological grounds may face genetic problems resulting from small effective size.


2020 ◽  
Vol 48 (2) ◽  
pp. 507-516 ◽  
Author(s):  
Pierre Hardouin ◽  
Adeline Goulet

Bacteriophages (phages) and their preys are engaged in an evolutionary arms race driving the co-adaptation of their attack and defense mechanisms. In this context, phages have evolved diverse anti-CRISPR proteins to evade the bacterial CRISPR–Cas immune system, and propagate. Anti-CRISPR proteins do not share much resemblance with each other and with proteins of known function, which raises intriguing questions particularly relating to their modes of action. In recent years, there have been many structure–function studies shedding light on different CRISPR–Cas inhibition strategies. As the anti-CRISPR field of research is rapidly growing, it is opportune to review the current knowledge on these proteins, with particular emphasis on the molecular strategies deployed to inactivate distinct steps of CRISPR–Cas immunity. Anti-CRISPR proteins can be orthosteric or allosteric inhibitors of CRISPR–Cas machineries, as well as enzymes that irreversibly modify CRISPR–Cas components. This repertoire of CRISPR–Cas inhibition mechanisms will likely expand in the future, providing fundamental knowledge on phage–bacteria interactions and offering great perspectives for the development of biotechnological tools to fine-tune CRISPR–Cas-based gene edition.


Author(s):  
T. N. Shafikova ◽  
Yu. V. Omelichkina

The study of plant defence mechanisms in response to pathogens in the mid-20th century resulted in Harold Flor’s gene-for-gene interaction hypothesis, which became recognised as central to the study of phytoimmunity. According to this theory, the outcome of interactions in plant – pathogen phytopathosystems – i.e. compatibility or incompatibility – is controlled genetically in interacting organisms and determined by the presence of specific genes in both pathogen and plant: resistance genes in the plant and avirulence genes in pathogen. The latest achievements in phytoimmunology, obtained with the help of modern molecular biology and bioinformatics methods, have made a significant contribution to the classical understanding of plant immunity and provided grounds for a modern concept of phytoimmunity consisting in the “zig-zag model” developed by Jonathan Jones and Jefferey Dangl. Plant immunity is currently understood as being determined by an innate multi-layer immune system involving various structures and mechanisms of specific and non-specific immunity. Recognition by plant membrane receptors of conservative molecular patterns associated with microorganisms, as well as molecules produced during cell wall disruption by pathogen hydrolytic enzymes forms a basic non-specific immune response in the plant. Detection of pathogen effector molecules by plant intra-cellular receptors triggers a specific effector-triggered immunity, resulting in the development of the hypersensitive response, systemic resistance and immune memory of the plant. Virulence factors and pathogen attack strategies on the one hand, and mechanisms of plant immune protection on the other, are the result of one form of constant co-evolution, often termed an “evolutionary arms race”. This paper discusses the main principles of Flor's classical “gene-for-gene interaction” theory as well as the molecular-genetic processes of plant innate immunity, their mechanisms and participants in light of contemporary achievements in phytoimmunology.


2010 ◽  
Vol 12 (1) ◽  
pp. 93-102 ◽  
Author(s):  
MICHAEL RAVENSDALE ◽  
ADNANE NEMRI ◽  
PETER H. THRALL ◽  
JEFFREY G. ELLIS ◽  
PETER N. DODDS

2010 ◽  
Vol 27 (11) ◽  
pp. 2555-2566 ◽  
Author(s):  
M. Fumagalli ◽  
R. Cagliani ◽  
S. Riva ◽  
U. Pozzoli ◽  
M. Biasin ◽  
...  

2012 ◽  
Vol 25 (5) ◽  
pp. 603-612 ◽  
Author(s):  
Edmund A. Quirin ◽  
Harpartap Mann ◽  
Rachel S. Meyer ◽  
Alessandra Traini ◽  
Maria Luisa Chiusano ◽  
...  

Cross-species comparative genomics approaches have been employed to map and clone many important disease resistance (R) genes from Solanum species—especially wild relatives of potato and tomato. These efforts will increase with the recent release of potato genome sequence and the impending release of tomato genome sequence. Most R genes belong to the prominent nucleotide binding site-leucine rich repeat (NBS-LRR) class and conserved NBS-LRR protein motifs enable survey of the R gene space of a plant genome by generation of resistance gene analogs (RGA), polymerase chain reaction fragments derived from R genes. We generated a collection of 97 RGA from the disease-resistant wild potato S. bulbocastanum, complementing smaller collections from other Solanum species. To further comparative genomics approaches, we combined all known Solanum RGA and cloned solanaceous NBS-LRR gene sequences, nearly 800 sequences in total, into a single meta-analysis. We defined R gene diversity bins that reflect both evolutionary relationships and DNA cross-hybridization results. The resulting framework is amendable and expandable, providing the research community with a common vocabulary for present and future study of R gene lineages. Through a series of sequence and hybridization experiments, we demonstrate that all tested R gene lineages are of ancient origin, are shared between Solanum species, and can be successfully accessed via comparative genomics approaches.


2021 ◽  
Author(s):  
Alita R. Burmeister ◽  
Rachel M. Sullivan ◽  
Jenna Gallie ◽  
Richard E. Lenski

AbstractBacteria often evolve resistance to phage through the loss or modification of cell-surface receptors. In Escherichia coli and phage λ, such resistance can catalyze a coevolutionary arms race focused on host and phage structures that interact at the outer membrane. Here, we analyze another facet of this arms race involving interactions at the inner membrane, whereby E. coli evolves mutations in mannose permease-encoding genes manY and manZ that impair λ’s ability to eject its DNA into the cytoplasm. We show that these man mutants arose concurrently with the arms race at the outer membrane. We tested the hypothesis that λ evolved an additional counter-defense that allowed them to infect bacteria with deleted man genes. The deletions severely impaired the ancestral λ, but some evolved phage grew well on the deletion mutants, indicating they regained infectivity by evolving the ability to infect hosts independently of the mannose permease. This coevolutionary arms race fulfills the model of an inverse-gene-for-gene infection network. Taken together, the interactions at both the outer and inner membranes reveal that coevolutionary arms races can be richer and more complex than is often appreciated.IMPACT STATEMENTLaboratory studies of coevolution help us understand how host defenses and pathogen counter-defenses change over time, which is often essential for predicting the future dynamics of host-pathogen interactions. One particular model, termed “inverse-gene-for-gene” coevolution, predicts that coevolution proceeds through alternating steps, whereby hosts lose the features exploited by pathogens, and pathogens evolve to exploit alternative features. Using a classic model system in molecular biology, we describe the nature and timing of a previously overlooked step in the coevolution of E. coli and bacteriophage lambda. Our work demonstrates that this mode of coevolution can profoundly re-shape the interactions between bacteria and phage.


2013 ◽  
Vol 26 (4) ◽  
pp. 398-406 ◽  
Author(s):  
Liesl Van der Linden ◽  
Jane Bredenkamp ◽  
Sanushka Naidoo ◽  
Joanne Fouché-Weich ◽  
Katherine J. Denby ◽  
...  

Bacterial wilt caused by Ralstonia solanacearum is a disease of widespread economic importance that affects numerous plant species, including Arabidopsis thaliana. We describe a pathosystem between A. thaliana and biovar 3 phylotype I strain BCCF402 of R. solanacearum isolated from Eucalyptus trees. A. thaliana accession Be-0 was susceptible and accession Kil-0 was tolerant. Kil-0 exhibited no wilting symptoms and no significant reduction in fitness (biomass, seed yield, and germination efficiency) after inoculation with R. solanacearum BCCF402, despite high bacterial numbers in planta. This was in contrast to the well-characterized resistance response in the accession Nd-1, which limits bacterial multiplication at early stages of infection and does not wilt. R. solanacearum BCCF402 was highly virulent because the susceptible accession Be-0 was completely wilted after inoculation. Genetic analyses, allelism studies with Nd-1, and RRS1 cleaved amplified polymorphic sequence marker analysis showed that the tolerance phenotype in Kil-0 was dependent upon the resistance gene RRS1. Knockout and complementation studies of the R. solanacearum BCCF402 effector PopP2 confirmed that the tolerance response in Kil-0 was dependent upon the RRS1–PopP2 interaction. Our data indicate that the gene-for-gene interaction between RRS1 and PopP2 can contribute to tolerance, as well as resistance, which makes it a useful model system for evolutionary studies of the arms race between plants and bacterial pathogens. In addition, the results alert biotechnologists to the risk that deployment of RRS1 in transgenic crops may result in persistence of the pathogen in the field.


2017 ◽  
Vol 16 (12) ◽  
pp. 2746-2760 ◽  
Author(s):  
Bao-hua WANG ◽  
Daniel J. Ebbole ◽  
Zong-hua WANG

2010 ◽  
Vol 365 (1544) ◽  
pp. 1153-1167 ◽  
Author(s):  
Laurence Loewe ◽  
William G. Hill

Population genetics is fundamental to our understanding of evolution, and mutations are essential raw materials for evolution. In this introduction to more detailed papers that follow, we aim to provide an oversight of the field. We review current knowledge on mutation rates and their harmful and beneficial effects on fitness and then consider theories that predict the fate of individual mutations or the consequences of mutation accumulation for quantitative traits. Many advances in the past built on models that treat the evolution of mutations at each DNA site independently, neglecting linkage of sites on chromosomes and interactions of effects between sites (epistasis). We review work that addresses these limitations, to predict how mutations interfere with each other. An understanding of the population genetics of mutations of individual loci and of traits affected by many loci helps in addressing many fundamental and applied questions: for example, how do organisms adapt to changing environments, how did sex evolve, which DNA sequences are medically important, why do we age, which genetic processes can generate new species or drive endangered species to extinction, and how should policy on levels of potentially harmful mutagens introduced into the environment by humans be determined?


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