Distinct Defense Research Articles

Role of the Staphylococcus aureus Extracellular Loop of GraS in Resistance to Distinct Human Defense Peptides in PMN and Invasive Cardiovascular infections.

GraS is a membrane sensor in Staphylococcus aureus that induces mprF and dltABCD expression to alter the surface positive charge upon exposure to cationic human defense peptides (HDPs). The sensing domain of GraS likely resides in the 9-residue extracellular loop (EL). In this study, we assessed a hospital-acquired methicillin-resistant S. aureus (HA-MRSA) strain (COL) for the specific role of two distinct EL mutations: F38G (bulk) and D/35/37/41K (charged inversion). Activation of mprF by polymyxin B (PMB) was reduced in the D35/37/41K mutant versus the D35/37/41G mutant, correlating with reduced surface positive charge; in contrast, these effects were less prominent in the F38G mutant but still lower than those in the parent. These data indicated that both electrostatic charge and steric bulk of the EL of GraS influence induction of genes impacting HDP resistance. Using mprF expression as a readout, we confirmed GraS signaling was pH dependent, increasing as pH was lowered (from pH 7.5 down to pH 5.5). In contrast to PMB activation, reduction of mprF was comparable at pH 5.5 between the P38G and D35/37/41K point mutants, indicating a mechanistic divergence between GraS activation by acidic pH versus cationic peptides. Survival assays in human blood and purified polymorphonuclear leukocytes (PMNs) revealed lower survival of the D35/37/41K mutant versus the F38G mutant, with both being lower than that of the parent. Virulence studies in the rabbit endocarditis model mirrored whole blood and PMN killing assay data described above. Collectively, these data confirmed the importance of specific residues within the EL of GraS in conferring essential bacterial responses for MRSA survival in infections.

Pore-forming toxins of foodborne pathogens.

Pore-forming toxins (PFTs) are water-soluble molecules that have been identified as the most crucial virulence factors during bacterial pathogenesis. PFTs disrupt the host cell membrane to internalize or to deliver other bacterial or virulence factors for establishing infections. Disruption of the host cell membrane by PFTs can lead to uncontrollable exchanges between the extracellular and the intracellular matrix, thereby disturbing the cellular homeostasis. Recent studies have provided insights into the molecular mechanism of PFTs during pathogenesis. Evidence also suggests the activation of several signal transduction pathways in the host cell on recognition of PFTs. Additionally, numerous distinctive host defense mechanisms as well as membrane repair mechanisms have been reported; however, studies reveal that PFTs aid in host immune evasion of the bacteria through numerous pathways. PFTs have been primarily associated with foodborne pathogens. Infection and death from diseases by consuming contaminated food are a constant threat to public health worldwide, affecting socioeconomic development. Moreover, the emergence of new foodborne pathogens has led to the rise of bacterial antimicrobial resistance affecting the population. Hence, this review focuses on the role of PFTs secreted by foodborne pathogens. The review highlights the molecular mechanism of foodborne bacterial PFTs, assisting bacterial survival from the host immune responses and understanding the downstream mechanism in the activation of various signaling pathways in the host upon PFT recognition. PFT research is a remarkable and an important field for exploring novel and broad applications of antimicrobial compounds as therapeutics.

Induction of pre‐chorismate, jasmonate and salicylate pathways byBurkholderiasp. RR18 in peanut seedlings

To characterize the mechanisms by which bacteria in the peanut rhizosphere promote plant growth and suppress Aspergillus niger, the fungus that causes collar rot of peanut. In all, 131 isolates cultured from the peanut rhizosphere were assayed for growth promotion in a seedling germination assay. The most effective isolate, RR18, was identified as Burkholderia sp. by 16S sequencing analysis. RR18 reduced collar rot disease incidence and increased the germination rate and biomass of peanut seeds, and had broad-spectrum antifungal activity. Quantitative analyses showed that RR18 induced long-lasting accumulation of jasmonic acid, salicylic acid and phenols, and triggered the activity of six defence enzymes related to these changes. Comparative proteomic analysis of treated and untreated seedlings revealed a clear induction of four abundant proteins, including a member of the pre-chorismate pathway, a regulator of clathrin-coated vesicles, a transcription factor and a hypothetical protein. Burkholderia sp. RR18 promotes peanut growth and disease resistance, and stably induces two distinct defence pathways associated with systemic resistance. This study demonstrates that a strain of the Burkholderia cepacia complex can elicit both salicylic- and jasmonic-acid-mediated defences, in addition to having numerous other beneficial properties.

Inflammatory Response Mechanisms of the Dentine-Pulp Complex and the Periapical Tissues.

The macroscopic and microscopic anatomy of the oral cavity is complex and unique in the human body. Soft-tissue structures are in close interaction with mineralized bone, but also dentine, cementum and enamel of our teeth. These are exposed to intense mechanical and chemical stress as well as to dense microbiologic colonization. Teeth are susceptible to damage, most commonly to caries, where microorganisms from the oral cavity degrade the mineralized tissues of enamel and dentine and invade the soft connective tissue at the core, the dental pulp. However, the pulp is well-equipped to sense and fend off bacteria and their products and mounts various and intricate defense mechanisms. The front rank is formed by a layer of odontoblasts, which line the pulp chamber towards the dentine. These highly specialized cells not only form mineralized tissue but exert important functions as barrier cells. They recognize pathogens early in the process, secrete antibacterial compounds and neutralize bacterial toxins, initiate the immune response and alert other key players of the host defense. As bacteria get closer to the pulp, additional cell types of the pulp, including fibroblasts, stem and immune cells, but also vascular and neuronal networks, contribute with a variety of distinct defense mechanisms, and inflammatory response mechanisms are critical for tissue homeostasis. Still, without therapeutic intervention, a deep carious lesion may lead to tissue necrosis, which allows bacteria to populate the root canal system and invade the periradicular bone via the apical foramen at the root tip. The periodontal tissues and alveolar bone react to the insult with an inflammatory response, most commonly by the formation of an apical granuloma. Healing can occur after pathogen removal, which is achieved by disinfection and obturation of the pulp space by root canal treatment. This review highlights the various mechanisms of pathogen recognition and defense of dental pulp cells and periradicular tissues, explains the different cell types involved in the immune response and discusses the mechanisms of healing and repair, pointing out the close links between inflammation and regeneration as well as between inflammation and potential malignant transformation.

Comparative transcriptomics and metabolomics in Vitis vinifera ‘Malvasia’ and Vitis rupestris ‘Du Lot’ cultured cells provide insights in possible innate resistance against pathogens

Grapevine varieties showing putative resistance to pathogens are a promising alternative to reduce the impact of disease management. Despite research efforts in understanding pathogen susceptibility/resistance to pathogens, the mechanisms that regulate these processes remain unclear. To identify the molecular and metabolic mechanisms associated with putative different susceptibility to pathogens and/or constitutive resistance, comparative transcriptomics and metabolomics were carried out in cultured cells of V. vinifera ‘Malvasia’ and V. rupestris ‘Du Lot’. Transcriptomic analysis revealed a higher enrichment of genes involved in biosynthesis of cell wall proteins, PR protein, ROS activation, phenylpropanoid pathway, TIR-NBS-LRR proteins and WRKY transcription factors in V. rupestris compared to V. vinifera. 1H-NMR based metabolomic analysis highlighted that leucine, isoleucine, valine, threonine, alanine, γ-aminobutyric acid (GABA), glutamine, phenylalanine and pyruvate significantly increased in V. rupestris compared to V. vinifera. Conversely, glucose, sucrose, and fumarate significantly decreased in V. rupestris compared to V. vinifera. Our findings reveal distinct pre-constitutive defense systems in two species consisting in an up-regulation of genes and primary metabolites involved in plant defense responses. These responses could be constitutively activated in V. rupestris opening new insights for sustainable viticulture through improved breeding programs.

The effects of aging on host resistance and disease tolerance to SARS-CoV-2 infection.

The ongoing coronavirus disease 2019 (COVID-19) crisis caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has triggered a large-scale pandemic that is afflicting millions of individuals in over 200 countries. The clinical spectrum caused by SARS-CoV-2 infections can range from asymptomatic infection to mild undifferentiated febrile illness to severe respiratory disease with multiple complications. Elderly patients (aged 60 and above) with comorbidities such as cardiovascular diseases and diabetes mellitus appear to be at highest risk of a severe disease outcome. To protect against pulmonary immunopathology caused by SARS-CoV-2 infection, the host primarily depends on two distinct defense strategies: resistance and disease tolerance. Resistance is the ability of the host to suppress and eliminate incoming viruses. By contrast, disease tolerance refers to host responses that promote host health regardless of their impact on viral replication. Disruption of either resistance or disease tolerance mechanisms or both could underpin predisposition to elevated risk of severe disease during viral infection. Aging can disrupt host resistance and disease tolerance by compromising immune functions, weakening of the unfolded protein response, progressive mitochondrial dysfunction, and altering metabolic processes. A comprehensive understanding of the molecular mechanisms underlying declining host defense in elderly individuals could thus pave the way to provide new opportunities and approaches for the treatment of severe COVID-19.

Discovery of multiple anti-CRISPRs highlights anti-defense gene clustering in mobile genetic elements

Many prokaryotes employ CRISPR–Cas systems to combat invading mobile genetic elements (MGEs). In response, some MGEs have developed strategies to bypass immunity, including anti-CRISPR (Acr) proteins; yet the diversity, distribution and spectrum of activity of this immune evasion strategy remain largely unknown. Here, we report the discovery of new Acrs by assaying candidate genes adjacent to a conserved Acr-associated (Aca) gene, aca5, against a panel of six type I systems: I–F (Pseudomonas, Pectobacterium, and Serratia), I–E (Pseudomonas and Serratia), and I–C (Pseudomonas). We uncover 11 type I–F and/or I–E anti-CRISPR genes encoded on chromosomal and extrachromosomal MGEs within Enterobacteriaceae and Pseudomonas, and an additional Aca (aca9). The acr genes not only associate with other acr genes, but also with genes encoding inhibitors of distinct bacterial defense systems. Thus, our findings highlight the potential exploitation of acr loci neighborhoods for the identification of previously undescribed anti-defense systems.

Contagious itch and disgust during a lecture on ectoparasitic infestations: Two co-activated complementary parasite defense systems?

(Audio-)visual itch transmission is referred to as "contagious itch" (CI) and has been linked to an evolutionarily ingrained ectoparasite defense system. Disgust is considered to be part of the behavioral immune system aimed to prevent the spreading of pathogens. Although they probably serve a similar purpose, the relationship between CI and disgust is unknown. We investigated their co-prevalence, correlation, and differences between the sexes and between skin-diseased and skin-healthy individuals. Medical students attending a lecture on ectoparasitic infestation indicated their change in itch and disgust compared to baseline on a 0 to 10 numerical rating scale (NRS) and specified which ectoparasitic infestation induced CI and disgust the most. Out of 132 participants, 87.9% reported CI, 84.1% disgust. The maximum intensity of CI was 3.68 ± 2.08 NRS (P < .0001), of disgust 3.80 ± 2.68 NRS (P < .0001), respectively. The CI and disgust correlated positively (rho 0.272; P = .002), but we also found that specific ectoparasitic infestations triggered rather itch than disgust and vice versa. Our results indicate that CI and disgust are coincident phenomena of distinct defense systems: CI is aimed to scrape off ectoparasites, disgust to prevent ingestion of pathogens. Furthermore, our data point to differences in CI and disgust between the sexes and skin-healthy vs skin-diseased participants.

TGF-β suppresses type 2 immunity to cancer.

The immune system uses two distinct defence strategies against infections: microbe-directed pathogen destruction characterized by type 1 immunity1, and host-directed pathogen containment exemplified by type 2 immunity in induction of tissue repair2. Similar to infectious diseases, cancer progresses with self-propagating cancer cells inflicting host-tissue damage. The immunological mechanisms of cancer cell destruction are well defined3-5, but whether immune-mediated cancer cell containment can be induced remains poorly understood. Here we show that depletion of transforming growth factor-β receptor 2 (TGFBR2) in CD4+ T cells, but not CD8+ T cells, halts cancer progression as a result of tissue healing and remodelling of the blood vasculature, causing cancer cell hypoxia and death in distant avascular regions. Notably, the host-directed protective response is dependent on the T helper 2 cytokine interleukin-4 (IL-4), but not the T helper 1 cytokine interferon-γ (IFN-γ). Thus, type 2 immunity can be mobilized as an effective tissue-level defence mechanism against cancer.

Muc2 Mucin and Nonmucin Microbiota Confer Distinct Innate Host Defense in Disease Susceptibility and Colonic Injury.

Background & AimsAlterations in intestinal MUC2 mucin and microbial diversity are closely linked with important intestinal pathologies; however, their impact on each other and on intestinal pathogenesis has been vaguely characterized. Therefore, it was of interest in this study to delineate distinct and cooperative function of commensal microbiota and the Muc2 mucus barrier in maintaining intestinal epithelial barrier function.MethodsMuc2 mucin deficient (Muc2–/–) and sufficient (Muc2+/+) littermates were used as a model for assessing the role of Muc2. To quantify the role of the microbiota in disease pathogenesis, Muc2+/+ and Muc2–/– littermates were treated with a cocktail of antibiotics that reduced indigenous bacteria, and then fecal transplanted with littermate stool and susceptibility to dextran sulphate sodium (DSS) quantified.ResultsAlthough, Muc2+/+ and Muc2–/– littermates share similar phyla distribution as evidenced by 16S sequencing they maintain their distinctive gastrointestinal phenotypes. Basally, Muc2–/– showed low-grade colonic inflammation with high populations of inflammatory and tolerogenic immune cells that became comparable to Muc2+/+ littermates following antibiotic treatment. Antibiotics treatment rendered Muc2+/+ but not Muc2–/– littermates highly susceptibility to DSS-induced colitis that was ILC3 dependent. Muc2–/– microbiota was colitogenic to Muc2+/+ as it worsened DSS-induced colitis. Microbiota dependent inflammation was confirmed by bone-marrow chimera studies, as Muc2–/– receiving Muc2+/+ bone marrow showed no difference in their susceptibility toward DSS induced colitis. Muc2–/– microbiota exhibited presence of characteristic OTUs of specific bacterial populations that were transferrable to Muc2+/+ littermates.ConclusionsThese results highlight a distinct role for Muc2 mucin in maintenance of healthy microbiota critical in shaping innate host defenses to promote intestinal homeostasis.

Distinct dietary cadmium toxic effects and defense strategies in two strains of gibel carp (Carassius gibelio) revealed by a comprehensive perspective

Previous studies demonstrated that gibel carp A strain was more susceptible to herpesvirus infection than other strains. Thus, we hypothesized that F strain might display better defense responses than the A strain against cadmium (Cd) exposure. To test our hypothesis, gibel carp A strain and F strain were exposed to three diets comprising of different concentrations of Cd for 8 weeks to compare their resistances to Cd. Comprehensive evaluations on biochemical, physiological and histological responses were conducted post-exposure. Results showed that no adverse effects and differences were observed on growth in two strains of gibel carp, compromising of the remarkable hepatoxicity-caused liver damage as shown by histological observations. Dietary Cd exposure stimulated antioxidant defense in the liver to counteract the Cd hepatoxicity, especially in the F strain. Activation of ER stress response positively stimulated the autophagy, then triggering apoptosis in fish after dietary Cd exposure. Thus, Cd-induced autophagy served as a protective strategy to alleviate hepatoxicity, but overaction of ER stress also triggered irreparable cell death via apoptosis. Cd induced dysregulation of lipid accumulation, which might be a common mechanism in response to hepatoxicity. Last but not least, the F strain showed stronger response on antioxidant, ER stress and autophagy, but apoptosis were remitted compared with the A strain, implying the F strain showed stronger response but better defense strategies to dietary Cd exposure. Our finding provides useful information for genetic breeding in aquaculture, and ultimately contribute to the safety assessment of aquatic products for human consumption.

Fluorescence measurements of the marine flatworm Macrostomum lignano during exposure to TNT and its derivatives 2-ADNT and 4-ADNT

Fluorescence measurements of the marine flatworm Macrostomum lignano were performed during exposure to the explosive TNT and its main derivatives 2-ADNT and 4-ADNT, using calcein AM, the acetoxymethylester of calcein, and the autofluorescence of its food (diatoms). Lethality was found to depend on temperature and exposure time. After 12 days of exposure to a concentration of 33,3 mg/L 2-ADNT and 4-ADNT, the lethality at 30 °C (100%) was strongly increased compared to 21 °C (~60%). First deaths were observed after four days of exposure. Using lower concentrations (≤3,33 mg/L) of all three compounds, the activity of ABC transporters (ATP binding cassette transporter) was determined using calcein as reporter dye. Worms exposed to toxicants for 72 h showed a significant upregulation of ABC transporter activity during exposure to 3,33 mg/L 2-ADNT and 4-ADNT, and 3 mg/L TNT demonstrating the efficacy of this cellular first line defense. A distinct behavioral defense of the worms decreased the uptake of 2-ADNT and 4-ADNT (0,033 mg/L) as they reduced feeding shown by diminished autofluorescence of algae in the gut.

Identification of New Anti-CRISPERS Uncovers Anti-Defense Gene Clustering

Many prokaryotes employ CRISPR-Cas systems to combat invading mobile genetic elements (MGEs). In response, MGEs have evolved Anti-CRISPR (Acr) proteins to bypass this immunity. Here, we describe the analysis of gene neighbors of the anti-CRISPR associated gene 5 (aca5) in search of new Acrs on chromosomal and extrachromosomal MGEs. Functional testing of candidates was performed against a panel of six type I systems, revealing 11 type I-F and/or I-E Acrs and a new aca (aca9). We find that acr genes not only associate with other acr genes, but also with inhibitors of distinct bacterial defense systems. These genomic regions appear to be “anti-defense islands”, reminiscent of the clustered arrangement of “defense islands” in prokaryotic genomes. Our findings expand on the diversity of CRISPR-Cas inhibitors and reveal the potential exploitation of acr loci neighborhoods for identifying new anti-defense systems.

The rice/maize pathogen Cochliobolus spp. infect and reproduce on Arabidopsis revealing differences in defensive phytohormone function between monocots and dicots.

The fungal genus Cochliobolus describes necrotrophic pathogens that give rise to significant losses on rice, wheat, and maize. Revealing plant mechanisms of non-host resistance (NHR) against Cochliobolus will help to uncover strategies that can be exploited in engineered cereals. Therefore, we developed a heterogeneous pathosystem and studied the ability of Cochliobolus to infect dicotyledons. We report here that C.miyabeanus and C.heterostrophus infect Arabidopsis accessions and produce functional conidia, thereby demonstrating the ability to accept Brassica spp. as host plants. Some ecotypes exhibited a high susceptibility, whereas others hindered the necrotrophic disease progression of the Cochliobolus strains. Natural variation in NHR among the tested Arabidopsis accessions can advance the identification of genetic loci that prime the plant's defence repertoire. We found that applied phytotoxin-containing conidial fluid extracts of C.miyabeanus caused necrotic lesions on rice leaves but provoked only minor irritations on Arabidopsis. This result implies that C.miyabeanus phytotoxins are insufficiently adapted to promote dicot colonization, which corresponds to a retarded infection progression. Previous studies on rice demonstrated that ethylene (ET) promotes C.miyabeanus infection, whereas salicylic acid (SA) and jasmonic acid (JA) exert a minor function. However, in Arabidopsis, we revealed that the genetic disruption of the ET and JA signalling pathways compromises basal resistance against Cochliobolus, whereas SA biosynthesis mutants showed a reduced susceptibility. Our results refer to the synergistic action of ET/JA and indicate distinct defence systems between Arabidopsis and rice to confine Cochliobolus propagation. Moreover, this heterogeneous pathosystem may help to reveal mechanisms of NHR and associated defensive genes against Cochliobolus infection.

Ontogenetic consistency in oak defence syndromes

Abstract Plant species allocate resources to multiple defensive traits simultaneously, often leading to so‐called defence syndromes (i.e. suites of traits that are co-expressed across several species). While reports of ontogenetic variation in plant defences are commonplace, no study to date has tested for ontogenetic shifts in defence syndromes, and we know little about the ecological and evolutionary drivers of variation in plant defence syndromes across ontogeny. We tested for ontogenetic variation in plant defence syndromes by measuring a suite of defensive and nutritional traits on saplings and adult trees of 29 oak (Quercus, Fagaceae) species distributed across Europe, North America, and Asia. In addition, we investigated if these syndromes exhibited a phylogenetic signal to elucidate the nature of their macro‐evolutionary variation, whether they were associated with levels of herbivore pressure and climatic conditions, and if any such evolutionary and ecological patterns were contingent on ontogeny. Our analyses revealed three distinct oak defence syndromes: the first included species with high defences, the second species with high defences and low nutrient levels, and the third species with high nutrients and thinner leaves. Interestingly, these defence syndromes remained virtually unchanged across the two ontogenetic stages sampled. In addition, our analyses indicated no evidence for a phylogenetic signal in oak syndromes, a result consistent across ontogenetic stages. Finally, with respect to ecological factors, we found no effect of climatic conditions on defences for either ontogenetic stage, whereas defence syndromes were associated with differing levels of herbivory in adults but not saplings suggesting an association between herbivore pressure and syndrome type that is contingent on ontogeny. Synthesis. Together, these findings indicate that defence syndromes remain remarkably consistent across oak ontogenetic stages, are evolutionarily labile, and while they appear unrelated to climate, they do appear to be associated with herbivory levels in an ontogenetic‐dependent manner. Overall, this study builds towards a better understanding of ecological and evolutionary factors underlying multivariate plant defensive phenotypes.

Commensal Bacteroidetes protect against Klebsiella pneumoniae colonization and transmission through IL-36 signalling.

The microbiota primes immune defences but the identity of specific commensal microbes which protect against infection is unclear. Conversely, how pathogens compete with the microbiota to establish their host niche is also poorly understood. Here, we investigate the antagonism between the microbiota and Klebsiella pneumoniae during colonization and transmission. We discover that maturation of the microbiota drives the development of distinct immune defence programs in the upper airway and intestine to limit K. pneumoniae colonization within these niches. Immune protection in the intestine depends on the development of Bacteroidetes, IL-36 signalling and macrophages. This effect of Bacteroidetes requires their conserved commensal colonization factor (CCF) polysaccharide utilization locus. Conversely, in the upper airway, Proteobacteria prime immunity through IL-17A, but K. pneumoniae overcomes these defences through encapsulation to effectively colonize this site. Ultimately, we find that host-to-host spread of K. pneumoniae occurs principally from its intestinal reservoir, and that CCF-producing Bacteroidetes are sufficient to prevent transmission between hosts through IL-36. Thus, our study provides mechanistic insight into when, where and how commensal Bacteroidetes protect against K. pneumoniae colonization and contagion, providing insight into how these protective microbes could be harnessed to confer population-level protection against K. pneumoniae infection.

Endospore Inactivation by Emerging Technologies: A Review of Target Structures and Inactivation Mechanisms.

Recent developments in preservation technologies allow for the delivery of food with nutritional value and superior taste. Of special interest are low-acid, shelf-stable foods in which the complete control or inactivation of bacterial endospores is the crucial step to ensure consumer safety. Relevant preservation methods can be classified into physicochemical or physical hurdles, and the latter can be subclassified into thermal and nonthermal processes. The underlying inactivation mechanisms for each of these physicochemical or physical processes impact different morphological or molecular structures essential for spore germination and integrity in the dormant state. This review provides an overview of distinct endospore defense mechanisms that affect emerging physical hurdles as well as which technologies address these mechanisms. The physical spore-inactivation technologies considered include thermal, dynamic, and isostatic high pressure and electromagnetic technologies, such as pulsed electric fields, UV light, cold atmospheric pressure plasma, and high- or low-energy electron beam.

Grapevine Phyllosphere Community Analysis in Response to Elicitor Application against Powdery Mildew.

The reduction of antimicrobial treatments and mainly the application of environmentally friendly compounds, such as resistance elicitors, is an impelling challenge to undertake more sustainable agriculture. We performed this research to study the effectiveness of non-conventional compounds in reducing leaf fungal attack and to investigate whether they influence the grape phyllosphere. Pathogenicity tests were conducted on potted Vitis vinifera “Nebbiolo” and “Moscato” cultivars infected with the powdery mildew agent (Erysiphe necator) and treated with three elicitors. Differences in the foliar microbial community were then evaluated by community-level physiological profiling by using BiologTM EcoPlates, high throughput sequencing of the Internal Transcribed Spacer (ITS) region, and RNA sequencing for the viral community. In both cultivars, all products were effective as they significantly reduced pathogen development. EcoPlate analysis and ITS sequencing showed that the microbial communities were not influenced by the alternative compound application, confirming their specific activity as plant defense elicitors. Nevertheless, “Moscato” plants were less susceptible to the disease and presented different phyllosphere composition, resulting in a richer viral community, when compared with the “Nebbiolo” plants. The observed effect on microbial communities pointed to the existence of distinct genotype-specific defense mechanisms independently of the elicitor application.

Geographically isolated Colorado potato beetle mediating distinct defense responses in potato is associated with the alteration of gut microbiota

Colorado potato beetle (CPB; Leptinotarsa decemlineata) has been detected in Xinjiang, China, since 1993 and has caused serious damage to potato production during its eastward expansion to new geographic ranges. Symbiotic bacteria often play an essential role for insects to exploit novel food sources and expand into otherwise inaccessible ecological niches. An important yet unresolved question is whether herbivore populations from different geographic ranges have distinct or equal abilities to adapt to plant-induced defenses. We examined whether two geographic CPB populations collected from Urumqi and Ili varied in triggering induced defenses in potato plants, and the results demonstrated that plants damaged by Ili CPB larvae showed higher levels/activities of the defensive protein polyphenol oxidase (PPO) than those damaged by Urumqi CPB larvae. Intriguingly, application of oral secretions (OS) from Ili CPB larvae triggered higher PPO activity in potato compared with the treatments by OS collected from Urumqi larvae. Moreover, higher counts of bacterial colonies were observed in Urumqi CPB larvae by traditional culturing and quantitative PCR. Comparing the gut bacterial composition of CPB individuals by 16S rRNA amplicon sequencing also revealed higher abundance and diversity of gut-associated bacteria in the Urumqi population than that in the Ili population. These results indicate that the gut bacteria of CPB larvae were geographically shaped during the process of invasion, which played an important role in mediating plant–insect interactions and possesses a great potential to drive further invasion.

The pan-immune system of bacteria: antiviral defence as a community resource.

Viruses and their hosts are engaged in a constant arms race leading to the evolution of antiviral defence mechanisms. Recent studies have revealed that the immune arsenal of bacteria against bacteriophages is much more diverse than previously envisioned. These discoveries have led to seemingly contradictory observations: on one hand, individual microorganisms often encode multiple distinct defence systems, some of which are acquired by horizontal gene transfer, alluding to their fitness benefit. On the other hand, defence systems are frequently lost from prokaryotic genomes on short evolutionary time scales, suggesting that they impose a fitness cost. In this Perspective article, we present the 'pan-immune system' model in which we suggest that, although a single strain cannot carry all possible defence systems owing to their burden on fitness, it can employ horizontal gene transfer to access immune defence mechanisms encoded by closely related strains. Thus, the 'effective' immune system is not the one encoded by the genome of a single microorganism but rather by its pan-genome, comprising the sum of all immune systems available for a microorganism to horizontally acquire and use.