Ancient microbial arms race sharpened our immune system—but also left us vulnerable

Science ◽  
2020 ◽  
Author(s):  
Ann Gibbons
Keyword(s):  

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.



2011 ◽  
Vol 85 (2) ◽  
pp. 113-120 ◽  
Author(s):  
M.J. Stear ◽  
D. Singleton ◽  
L. Matthews

AbstractThe purpose of this paper was to discuss from an evolutionary perspective the interaction between domestic sheep (Ovis aries)and their gastrointestinal nematodes. Although evolution is the central theme of biology, there has been little attempt to consider how evolutionary forces have shaped and continue to shape the relationships between domestic animals and their parasite community. Mathematical modelling of the host–parasite relationship indicated that the system is remarkably robust to perturbations in its parameters. This robustness may be a consequence of the long coevolution of host and parasites. Although nematodes can potentially evolve faster than the host, coevolution is not dominated by the parasite and there are several examples where breeds of cattle or sheep have evolved high levels of resistance to disease. Coevolution is a more equal partnership between host and nematode than is commonly assumed. Coevolution between parasites and the host immune system is often described as an arms race where both host immune response genes and parasite proteins evolve rapidly in response to each other. However, initial results indicate that nematode antigens are not evolving rapidly; the arms race between the immune system and nematodes, if it exists, is happening very slowly. Fisher's fundamental theorem of natural selection states that genes with positive effects on fitness will be fixed by natural selection. Consequently, heritable variation in fitness traits is expected to be low. Contrary to this argument, there is considerable genetic variation in resistance to nematode infection. In particular, the heritabilities of nematode-specific IgA and IgE activity are moderate to high. The reasons for this apparent violation of the fundamental theorem of natural selection are not clear but several possible explanations are explored. Faecal nematode egg counts increase at the beginning of the grazing season – a phenomenon known as the periparturient rise. This increase benefits host and parasite and appears to be a consequence of coevolution. In conclusion, an evolutionary perspective can shed light on many aspects of the host–parasite relationship in domestic animals.



2019 ◽  
Vol 73 (1) ◽  
pp. 667-696 ◽  
Author(s):  
Yan Wang ◽  
Brett M. Tyler ◽  
Yuanchao Wang

Plant-pathogenic oomycetes include numerous species that are ongoing threats to agriculture and natural ecosystems. Understanding the molecular dialogs between oomycetes and plants is instrumental for sustaining effective disease control. Plants respond to oomycete infection by multiple defense actions including strengthening of physical barriers, production of antimicrobial molecules, and programmed cell death. These responses are tightly controlled and integrated via a three-layered immune system consisting of a multiplex recognition layer, a resilient signal-integration layer, and a diverse defense-action layer. Adapted oomycete pathogens utilize apoplastic and intracellular effector arsenals to counter plant immunity mechanisms within each layer, including by evasion or suppression of recognition, interference with numerous signaling components, and neutralization or suppression of defense actions. A coevolutionary arms race continually drives the emergence of new mechanisms of plant defense and oomycete counterdefense.



2016 ◽  
Vol 198 (6) ◽  
pp. 941-950 ◽  
Author(s):  
Inbal Maniv ◽  
Wenyan Jiang ◽  
David Bikard ◽  
Luciano A. Marraffini

ABSTRACTClustered regularly interspaced short palindromic repeat (CRISPR) loci encode an adaptive immune system of prokaryotes. Within these loci, sequences intercalated between repeats known as “spacers” specify the targets of CRISPR immunity. The majority of spacers match sequences present in phages and plasmids; however, it is not known whether there are differences in the immunity provided against these diverse invaders. We studied this issue using theStaphylococcus epidermidisCRISPR system, which harbors spacers matching both phages and plasmids. We determined that this CRISPR system provides similar levels of defense against the conjugative plasmid pG0400 and the bacteriophage CNPX. However, whereas antiplasmid immunity was very sensitive to the introduction of mismatches in the target sequence, mutations in the phage target were largely tolerated. Placing the phage and plasmid targets into a vector that can be both conjugated and transduced, we demonstrated that the route of entry of the target has no impact on the effect of the mismatches on immunity. Instead, we established that the specific sequences of each spacer/target determine the susceptibility of theS. epidermidisCRISPR system to mutations. Therefore, spacers that are more resistant to mismatches would provide long-term immunity against phages and plasmids that otherwise would escape CRISPR targeting through the accumulation of mutations in the target sequence. These results uncover an unexpected complexity in the arms race between CRISPR-Cas systems and prokaryotic infectious genetic elements.IMPORTANCECRISPR-Cas loci protect bacteria and archaea from both phage infection and plasmid invasion. These loci harbor short sequences of phage and plasmid origin known as “spacers” that specify the targets of CRISPR-Cas immunity. The presence of a spacer sequence matching a phage or plasmid ensures host immunity against infection by these genetic elements. In turn, phages and plasmids constantly mutate their targets to avoid recognition by the spacers of the CRISPR-Cas immune system. In this study, we demonstrated that different spacer sequences vary in their ability to tolerate target mutations that allow phages and plasmids to escape from CRISPR-Cas immunity. These results uncover an unexpected complexity in the arms race between CRISPR-Cas systems and prokaryotic infectious genetic elements.



Evolution ◽  
2012 ◽  
Vol 66 (8) ◽  
pp. 2528-2539 ◽  
Author(s):  
Olivia Roth ◽  
Isabel Keller ◽  
Susanne H. Landis ◽  
Walter Salzburger ◽  
Thorsten B.H. Reusch


2017 ◽  
Author(s):  
Jake L Weissman ◽  
Rayshawn Holmes ◽  
Rodolphe Barrangou ◽  
Sylvain Moineau ◽  
William F Fagan ◽  
...  

AbstractBacteria and their viral pathogens face constant pressure for augmented immune and infective capabilities, respectively. Under this reciprocally imposed selective regime, we expect to see a runaway evolutionary arms race, ultimately leading to the extinction of one species. Despite this prediction, in many systems host and pathogen coexist with minimal coevolution even when well-mixed. Previous work explained this puzzling phenomenon by invoking fitness tradeoffs, which can diminish an arms race dynamic. Here we propose that the regular loss of immunity by the bacterial host can also produce host-phage coexistence. We pair a general model of immunity with an experimental and theoretical case study of the CRISPR-Cas immune system to contrast the behavior of tradeoff and loss mechanisms in well-mixed systems. We find that, while both mechanisms can produce stable coexistence, only immune loss does so robustly within realistic parameter ranges.



2012 ◽  
Vol 33 (1) ◽  
pp. 15
Author(s):  
David Guest

Unlike animals, plants cannot flee, fight or hide from predators. Plants lack mobile defender cells or an adaptive immune system and have instead evolved defences based on pre-formed barriers and inducible cellular responses regulated by local and systemic signals. The interaction between pathogen effectors and these defences sets up an intriguing molecular arms race between plants and pathogenic fungi, bacteria, viruses, viroids and nematodes.



eLife ◽  
2015 ◽  
Vol 4 ◽  
Author(s):  
Edward N Baker ◽  
Paul G Young

Bacterial surface proteins covalently attach to host cells via a mechanism that is also used by immune system proteins that help eliminate invading pathogens.



2019 ◽  
Author(s):  
soumya banerjee

Crime is analogous to a pathogenic infection and the policeresponse to it is similar to an immune response. Moreover, the biological immune system is also engaged in an arms race with pathogens. These analogies enable an immune systeminspired theory of crime and violence in human societies, especially in large agglomerations like cities.An immune system inspired theory of crime can provide a new perspective on the dynamics of violence in societies. The competitive dynamics between police and criminals hassimilarities to how the immune system is involved in an arms race with invading pathogens. Cities have properties similar to biological organisms - the police and military forces wouldbe the immune system that protects against invading internal and external forces.The arms race between immune system and pathogens is similar to the competitive dynamics between police and criminals. Cities have properties similar to biological organisms and in this theory the police and military would be the immune system that protects against bothinternal and external forces.



2021 ◽  
Vol 12 ◽  
Author(s):  
Chalita Chomkatekaew ◽  
Phumrapee Boonklang ◽  
Apiwat Sangphukieo ◽  
Claire Chewapreecha


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