Host Colonization Research Articles

Triple Threat: How Global Fungal Rice and Wheat Pathogens Utilize Comparable Pathogenicity Mechanisms to Drive Host Colonization.

Plant pathogens pose significant threats to global cereal crop production, particularly for essential crops like rice and wheat, which are fundamental to global food security and provide nearly 40% of the global caloric intake. As the global population continues to rise, increasing agricultural production to meet food demands becomes even more critical. However, the production of these vital crops is constantly threatened by phytopathological diseases, especially those caused by fungal pathogens such as Magnaporthe oryzae, the causative agent of rice blast disease, Fusarium graminearum, responsible for Fusarium head blight (FHB) in wheat, and Zymoseptoria tritici, the source of Septoria tritici blotch (STB). All three pathogens are hemibiotrophic, initially colonizing the host through a biotrophic, symptomless lifestyle, followed by causing cell death through the necrotrophic phase. Additionally, they deploy a diverse range of effectors, including proteinaceous and non-proteinaceous molecules, to manipulate fundamental host cellular processes, evade immune responses, and promote disease progression. This review discusses recent advances in understanding the effector biology of these three pathogens, highlighting both the shared functionalities and unique molecular mechanisms they employ to regulate conserved elements of host pathways, such as directly manipulating gene transcription in host nuclei, disrupting reactive oxygen species (ROS) signaling, interfering with protein stability, and undermining host structural integrity. By detailing these complex interactions, the review explores potential targets for innovative control measures and emphasizes the need for further research to develop effective strategies against these destructive pathogens in the face of evolving environmental and agricultural challenges.

Non-coding RNA Networks in Infection.

In the face of global health challenges posed by infectious diseases and the emergence of drug-resistant pathogens, the exploration of cellular non-coding RNA (ncRNA) networks has unveiled new dimensions in infection research. Particularly microRNAs (miRNAs) and long non-coding RNAs (lncRNAs) have emerged as instrumental players in ensuring a balance between protection against hyper-inflammatory conditions and the effective elimination of pathogens. Specifically, ncRNAs, such as the miRNA miR-155 or the lncRNAs MaIL1 (macrophage interferon-regulatory lncRNA 1), and LUCAT1 (lung cancer-associated transcript 1) have been recurrently linked to infectious and inflammatory diseases. Together with other ncRNAs, discussed in this chapter, they form a complex regulatory network shaping the host response to pathogens. Additionally, some pathogens exploit these ncRNAs to establish and sustain infections, underscoring their dual roles in host protection and colonization. Despite the substantial progress made, the vast majority of ncRNA loci remains unexplored, with ongoing research likely to reveal novel ncRNA categories and expand our understanding of their roles in infections. This chapter consolidates current insights into ncRNA-mediated regulatory networks, highlighting their contributions to severe diseases and their potential as targets and biomarkers for innovative therapeutic strategies.

Pseudovibriamides from Pseudovibrio marine sponge bacteria promote flagellar motility via transcriptional modulation.

Pseudovibrio α-Proteobacteria have been repeatedly isolated from marine sponges and proposed to be beneficial to the host. Bacterial motility is known to contribute to host colonization. We have previously identified pseudovibriamides A and B, produced in culture by Pseudovibrio brasiliensis Ab134, and shown that pseudovibriamide A promotes flagellar motility. Pseudovibriamides are encoded in a hybrid nonribosomal peptide synthetase-polyketide synthase gene cluster that also includes several accessory genes. Pseudovibriamide A is a linear heptapeptide and pseudovibriamide B is a nonadepsipeptide derived from pseudovibriamide A. Here, we define the borders of the pseudovibriamides gene cluster, assign function to biosynthetic genes using reverse genetics, and test the hypothesis that pseudovibriamides impact motility by modulating gene transcription. RNA-sequencing transcriptomic analyses of strains having different compositions of pseudovibriamides suggested that both pseudovibriamides A and B affect genes potentially involved in motility, and that a compensatory mechanism is at play in mutants that produce only pseudovibriamide A, resulting in comparable flagellar motility as the wild type. The data gathered suggest that pseudovibriamides A and B have opposite roles in modulating a subset of genes, with pseudovibriamide B having a primary effect in gene activation, and pseudovibriamide A on inhibition. Finally, we observed many differentially expressed genes (up to 29% of the total gene number) indicating that pseudovibriamides have a global effect on transcription that goes beyond motility.IMPORTANCEMarine sponges are found throughout the oceans from tropical coral reefs to polar sea floors, playing crucial roles in marine ecosystems. Pseudovibrio bacteria have been proposed to contribute to sponge health. We have previously shown that pseudovibriamides produced by Pseudovibrio brasiliensis promote bacterial motility, a behavior that is beneficial to bacterial survival and host colonization. The gene cluster that encodes pseudovibriamide biosynthesis is found in two-thirds of Pseudovibrio genomes. This gene cluster is also present in Pseudomonas bacteria that interact with terrestrial plants and animals. Here, we first assign functions to pseudovibriamide biosynthetic genes using reverse genetics. We then show that pseudovibriamides play a major role in transcriptional regulation, affecting up to 29% of P. brasiliensis genes, including motility genes. Thus, this work gives insights into pseudovibriamide biosynthesis and provides evidence that they are signaling molecules relevant to bacterial motility and to other yet-to-be-identified phenotypes.

A pipeline for validation of Serendipita indica effector-like sRNA suggests cross-kingdom communication in the symbiosis with Arabidopsis.

Bidirectional communication between pathogenic microbes and their plant hosts via small (s)RNA-mediated cross-kingdom RNA interference (ckRNAi) is a key element for successful host colonisation. Whether mutualistic fungi of the Serendipitaceae family, known for their extremely broad host range, use sRNAs to colonize plant roots is still under debate. To address this question, we developed a pipeline to validate the accumulation, translocation, and activity of fungal sRNAs in post-transcriptional silencing of Arabidopsis thaliana genes. Using stem-loop RT-qPCR, we detected the expression of a specific set of Serendipita indica (Si)sRNAs, targeting host genes involved in cell wall organization, hormonal signalling regulation, immunity, and gene regulation. To confirm the gene silencing activity of these sRNAs in plant cells, SisRNAs were transiently expressed in protoplasts. Stem-loop PCR confirmed sRNAs expression and accumulation, while qPCR validated post-transcriptional gene silencing of their predicted target genes. Furthermore, Arabidopsis ARGONAUTE 1 immunoprecipitation (AtAGO1-IP) revealed the loading of fungal SisRNAs into the plant RNAi machinery, suggesting the translocation of SisRNA from the fungus into root cells. In conclusion, this study provides a blueprint for rapid selection and analysis of sRNA effectors and further supports the model of cross-kingdom communication in the Sebacinoid symbiosis.

Host plant selection and performance of ambrosia beetles in flood-stressed versus ethanol-injected trees provide implications for management strategies

Abstract Ambrosia beetles (Curculionidae: Scolytinae and Platypodinae) are fungus-farming woodborers that can cause damage to the trees they colonize. Some of these beetles target stressed plants that emit ethanol, and management strategies have proposed using ethanol-injected trees as trap trees to monitor or divert dispersing adult females away from valuable crops. In this study, we used container-grown trees from 8 species to compare the effect of ethanol injection versus flooding on ambrosia beetle host selection and colonization success. Our aims were to understand whether ethanol injection is a suitable technique for different ambrosia beetle species and whether its effectiveness varies depending on the tree species used. In addition, we quantified the amount of ethanol in tree tissues to understand whether ethanol concentration could reflect observed differences among treatments and tree species. Our findings demonstrated that ethanol-injected trees were significantly more selected by both Xyleborinus saxesenii and Xylosandrus spp. and that significantly more adult beetles of both taxa emerged from ethanol-injected than flood-stressed trees. In addition, we showed that ethanol injection can trigger attacks by X. saxesenii and Xylosandrus spp. on a variety of deciduous tree species, nullifying the effects of the species-specific characteristics observed on flood-stressed trees, which can only partially be attributed to the amount of ethanol within the plant. This supported the idea that practitioners can potentially select any species of deciduous trees in management programs for ambrosia beetles based on ethanol-injected trees.

Inferior Caballeronia symbiont lacks conserved symbiosis genes.

Pentatomomorphan bugs can form symbiotic associations with bacteria belonging to the supergenus Burkholderia sensu lato. This relationship has become a model for understanding environmental symbiont acquisition. Host insects can utilize various symbiont strains from across Burkholderia sensu lato; however, host colonization success and benefits conferred vary by bacterial clade. Therefore, we conducted a meta-analysis aimed at identifying candidate genes that underpin beneficial symbioses within this system. We scanned the entire Burkholderiaceae family for the presence of 17 colonization-associated genes, as well as 88 candidate genes that are differentially expressed during symbiosis. There was no difference in the distribution of the 17 colonization-associated genes between symbiotic (Caballeronia and insect-associated plant beneficial and environmental clade) and non-symbiotic lineages; however, there was a higher prevalence of the 88 candidate genes in the insect symbiont lineages. We subsequently analysed the genomes of nine symbiotic Caballeronia species that confer varying fitness benefits to their insect hosts. One symbiont species was significantly worse, one was significantly better and the remaining seven were intermediate in terms of conferred host fitness benefits. We found that species possessing a higher number of the candidate genes conferred faster host development time. Furthermore, we identified two candidate genes that were missing in the least beneficial species but present in the other eight, suggesting that these genes may be important in modulating symbiont quality. Our study suggests that the mechanisms required for host colonization are broadly distributed across Burkholderiaceae, but the genes that determine symbiont quality are more prevalent in insect-associated species. This work helps to identify genes that influence this highly specialized yet diverse symbiosis between Pentatomomorphan insects and Burkholderiaceae bacteria.

QPCR-based quantification reveals high plant host-specificity of endophytic colonization levels in leaves.

Despite the high functional importance of endophytes, we still have limited understanding of the biotic and abiotic factors that influence colonization of plant hosts along major ecological gradients and lack quantitative estimates of their colonization extent. In this study, we hypothesized that the developmental stage of the ecosystem will affect the levels of bacterial and fungal endophytic assemblages in the foliar endosphere. We quantified levels of bacterial and fungal endophytes in leaves of four plant hosts at four stages of vegetation succession using an optimized qPCR protocol with bacteria-specific 16S and fungi-targeting primers. (1) The ecosystem developmental stage did not have a significant effect on the colonization levels of bacterial or fungal endophytes. (2) Colonization levels by bacterial and fungal endophytes were governed by different mechanisms. (3) Endophytic colonization levels and their relationship to foliar tissue stoichiometry were highly host specific. Quantifying colonization levels is important in the study of endophytic ecology, and the fast, relatively low-cost qPCR-based method can supply useful ecological information, which can significantly enhance the interpretation potential of descriptive data generated, for example, by next-generation sequencing.

The Campylobacter jejuni BumS sensor phosphatase detects the branched short-chain fatty acids isobutyrate and isovalerate as direct cues for signal transduction.

Two-component signal transduction systems (TCSs) are nearly ubiquitous across bacterial species and enable bacteria to sense and respond to specific cues for environmental adaptation. The Campylobacter jejuni BumSR TCS is unusual in that the BumS sensor exclusively functions as a phosphatase rather than a kinase to control phosphorylated levels of its cognate BumR response regulator (P-BumR). We previously found that BumSR directs a response to the short-chain fatty acid butyrate generated by resident microbiota so that C. jejuni identifies ideal lower intestinal niches in avian and human hosts for colonization. However, butyrate is an indirect cue for BumS and did not inhibit in vitro BumS phosphatase activity for P-BumR. In this work, we expanded the repertoire of lower intestinal metabolites that are cues sensed by BumS that modulate the expression of genes required for colonization to include the branched short-chain fatty acids isobutyrate and isovalerate. Unlike butyrate, isobutyrate and isovalerate inhibited in vitro BumS phosphatase activity for P-BumR, indicating that these metabolites are direct cues for BumS. Isobutyrate and isovalerate reduced the thermostability of BumS and caused a reorganization of protein structure to suggest how sensing these cues inhibits phosphatase activity. We also identified residues in the BumS sensory domain required to detect isobutyrate, isovalerate, and butyrate and for optimal colonization of hosts to reveal how gut bacteria can recognize these intestinal metabolites. Our work reveals how this unusual bacterial sensor phosphatase senses a repertoire of intestinal metabolites and how cues alter BumSR signal transduction to influence C. jejuni colonization of hosts.IMPORTANCETCSs are prevalent in many bacteria, but the cues sensed by each are not actually known for many of these systems. Microbiota-generated butyrate in human and avian hosts is detected by the Campylobacter jejuni BumS sensor phosphatase so that the bacterium identifies ideal lower intestinal niches for colonization. However, BumS only indirectly senses butyrate to inhibit dephosphorylation of its cognate BumR response regulator. Here, we expanded the repertoire of cues sensed by BumS to the branched-short chain fatty acids isobutyrate and isovalerate that are also abundant in the lower intestines. Both isobutyrate and isovalerate are potent, direct cues for BumS, whereas butyrate is an indirect cue. Leveraging isobutyrate and isovalerate as direct cues, we reveal BumS structure is altered upon cue detection to inhibit its phosphatase activity. We provide an understanding of the mechanics of an unusual mode of signal transduction executed by BumSR and other bacterial sensor phosphatase-driven TCSs.

Reciprocal regulation between bacterial secretion systems and host metabolism: Enhancing bacterial intracellular survival capability.

Secretion systems are intricate nanomachines present on many bacterial cell membranes that deliver various bacterially-encoded effector proteins into eukaryotic or prokaryotic cells. They are pivotal in bacterial invasion, host colonization, and pathogenesis. After infection, bacteria employ these machines to deliver toxic effectors to the cytoplasm of host cells that disrupt their metabolic balance, such as interfering with glucose metabolism, promoting lipid droplets formation, altering amino acid profiles and mitochondrial morphology, and reducing ROS levels, to ensure bacterial intracellular survival. Furthermore, metabolites within host cells can modulate the expression and/or function of bacterial secretion systems. This review summarizes recent advancements in understanding the impact of bacterial secretion systems on host cell metabolism and the feedback regulation of host metabolites on these machines, providing novel perspectives on host-pathogen interactions and mechanisms of bacterial pathogenesis.

Identification and genomic insights into Bacillus siamensis strains with host colonization potential and activity against tomato bacterial wilt.

Bacterial wilt (BW), caused by Ralstonia solanacearum species complex (RSSC), is considered as one of the most destructive plant diseases worldwide. In this study, two strains of Bacillus siamensis, BB605-1 and BB653, were screened and identified from endophytes in healthy tomato and mangrove plants, respectively. Both strains demonstrated antagonistic activities against all 16 RSSC strains, representing eight sequevars from various hosts. The growth of RSSC was suppressed by the crude antimicrobial extracts produced by two strains. The pot inoculation experiment revealed the control efficiencies of two strains against tomato bacterial wilt as 59.63% and 63.98%, respectively. After imparting rifampicin resistance to the strains and applying them to tomato plants, both strains successfully established stable colonization in the rhizosphere, roots, stems, and leaves of tomato plants. Additionally, our study demonstrated that both strains exhibited significant plant growth-promoting properties. Complete genome sequencing revealed genome size of 3.868 M bp with 3594 protein-coding genes for BB605-1, and 3.857 M bp with 3600 protein-coding genes for BB653. Genome analysis of both strains identified seven secondary metabolite clusters with known antimicrobial properties and predicted three unknown compounds with potentially novel properties. Genome mining revealed several key genes associated with plant growth regulation, colonization, and biofilm formation, and we also detected these corresponding substances. These findings provide a compelling case for the application of B. siamensis in agricultural practices. The isolates' multiple capacities to colonize, enhance plant growth, and exert antagonistic effects against BW positions them as highly promising candidates for an integrated biological solution. © 2024 Society of Chemical Industry.

Allosteric substrate release by a sialic acid TRAP transporter substrate binding protein

The tripartite ATP-independent periplasmic (TRAP) transporters enable Vibrio cholerae and Haemophilus influenzae to acquire sialic acid, aiding their colonization of human hosts. This process depends on SiaP, a substrate-binding protein (SBP) that captures and delivers sialic acid to the transporter. We identified 11 nanobodies that bind specifically to the SiaP proteins from H. influenzae (HiSiaP) and V. cholerae (VcSiaP). Two nanobodies inhibited sialic acid binding. Detailed structural and biophysical studies of one nanobody-SBP complex revealed an allosteric inhibition mechanism, preventing ligand binding and releasing pre-bound sialic acid. A hydrophobic surface pocket of the SBP is crucial for the allosteric mechanism and for the conformational rearrangement that occurs upon binding of sialic acid to the SBP. Our findings provide new clues regarding the mechanism of TRAP transporters, as well as potential starting points for novel drug design approaches to starve these human pathogens of important host-derived molecules.

The Zymoseptoria tritici effector Zt-11 contributes to aggressiveness in wheat.

Zymoseptoria tritici is an ascomycete fungus and the causal agent of Septoria tritici leaf blotch (STB) in wheat. Z. tritici secretes an array of effector proteins that are likely to facilitate host infection, colonisation and pycnidia production. In this study we demonstrate a role for Zt-11 as a Z. tritici effector during disease progression. Zt-11 is upregulated during the transition of the pathogen from the biotrophic to necrotrophic phase of wheat infection. Deletion of Zt-11 delayed disease development in wheat, reducing the number and size of pycnidia, as well as the number of macropycnidiospores produced by Z. tritici. This delayed disease development by the ΔZt-11 mutants was accompanied by a lower induction of PR genes in wheat, when compared to infection with wildtype Z. tritici. Overall, these data suggest that Zt-11 plays a role in Z. tritici aggressiveness and STB disease progression possibly via a salicylic acid associated pathway.

Evolution of the CRISPR-Cas9 defence system in Mycoplasma gallisepticum following colonization of a novel bird host.

Clustered regularly interspaced short palindromic repeat (CRISPR)-Cas systems are bacterial defences that target bacteriophages and mobile genetic elements. How these defences evolve in novel host environments remains largely unknown. We studied the evolution of the CRISPR-Cas system in Mycoplasma gallisepticum (also named Mycoplasmoides gallisepticum), a bacterial pathogen of poultry that jumped into a passerine host ~30 years ago. Over the decade following the host shift, all isolates displaying a functional CRISPR-Cas system were found not only to harbour completely new sets of spacers, but the DNA protospacer adjacent motif recognized by the main effector M. gallisepticum Cas9 (MgCas9) was also different. These changes in CRISPR-Cas diversity and specificity are consistent with a change in the community of phages and mobile elements infecting M. gallisepticum as it colonized the novel host. In the years following the host shift, we also detected a gradual rise in isolates displaying non-functional MgCas9. After 12 years, all circulating isolates harboured inactive forms only. This loss of CRISPR-Cas function comes at a time when the passerine host is known to have evolved widespread resistance, which in turn drove the evolution of increasing M. gallisepticum virulence through antagonistic coevolution. Such striking concordance in the rise of inactivated forms of CRISPR-Cas and the evolution of host resistance suggests that the inactivation of the CRISPR-Cas system was necessary for enabling adaptive bacterial responses to host-driven selection. We highlight the need to consider both host and pathogen selection pressures on bacteria for understanding the evolution of CRISPR-Cas systems and the key factors driving the emergence of a pathogenic bacterium in a novel host.

Vibrio cholerae CsrA controls ToxR levels by increasing the stability and translation of toxR mRNA.

Intestinal colonization and virulence factor production in response to environmental cues is mediated through several regulatory factors in Vibrio cholerae, including the highly conserved RNA-binding global regulatory protein CsrA. We have shown previously that CsrA increases synthesis of the virulence-associated transcription factor ToxR in response to specific amino acids (NRES) and is required for the virulence of V. cholerae in the infant mouse model of cholera. In this study, we mapped the 5' untranslated region (5' UTR) of toxR and showed that CsrA can bind directly to an RNA sequence encompassing the 5' UTR, indicating that the regulation of ToxR levels by CsrA is direct. Consistent with this observation, the 5' UTR of toxR contains multiple putative CsrA binding sequences (GGA motifs), and mutating these motifs disrupted the CsrA-mediated increase in ToxR. Optimal binding of CsrA to a defined RNA oligonucleotide required the bridging of two GGA motifs within a single RNA strand. To determine the mechanism of regulation by CsrA, we assayed toxR transcript levels, stability, and efficiency of translation. Both the amount of toxR mRNA in NRES and the stability of the toxR transcript were increased by CsrA. Using an in vitro translation assay, we further showed that synthesis of ToxR was greatly enhanced in the presence of purified CsrA, suggesting a direct role for CsrA in the translation of toxR mRNA. We propose a model in which CsrA binding to the 5' UTR of the toxR transcript promotes ribosomal access while precluding interactions with RNA-degrading enzymes.IMPORTANCEVibrio cholerae is uniquely adapted to marine environments as well as the human intestinal tract. Global regulators, such as CsrA, which help translate environmental cues into an appropriate cellular response, are critical for switching between these distinct environments. Understanding the pathways involved in relaying environmental signals is essential for understanding both the environmental persistence and the intestinal pathogenesis of this devastating human pathogen. In this study, we demonstrate that CsrA directly regulates the synthesis of ToxR, a key virulence factor of V. cholerae. Under conditions favoring high levels of active CsrA in the cell, such as in the presence of particular amino acids, CsrA increases ToxR protein levels by binding to the toxR transcript and enhancing both its stability and translation. By responding to nutrient availability, CsrA is perfectly poised to activate the virulence gene regulatory cascade at the preferred site of colonization in the human host, the nutrient-rich small intestinal mucosa.

Cyclic Diguanylate in the Wild: Roles During Plant and Animal Colonization.

Cyclic diguanylate (c-di-GMP) is a near-ubiquitous signaling molecule that regulates the motility-to-sessility transition in many bacterial species. Among the phenotypes influenced by c-di-GMP are biofilm formation, motility, cell cycle, and virulence. The hallmark phenotypes regulated by c-di-GMP-biofilm formation and motility-are key determinants of host-bacterial interactions. A large body of research has identified the roles of c-di-GMP in regulating phenotypes in culture. While numerous studies have investigated roles for c-di-GMP during the establishment and maintenance of pathogenic host-bacterial associations, considerably less attention has been devoted to defining the roles of c-di-GMP during beneficial and commensal associations. This review describes the known roles of c-di-GMP in regulating phenotypes that contribute to host colonization, with a focus on knowledge gaps and future prospects for examining c-di-GMP during beneficial colonization.

SntB triggers the antioxidant pathways to regulate development and aflatoxin biosynthesis in Aspergillus flavus.

The epigenetic reader SntB was identified as an important transcriptional regulator of growth, development, and secondary metabolite synthesis in Aspergillus flavus. However, the underlying molecular mechanism is still unclear. In this study, by gene deletion and complementation, we found SntB is essential for mycelia growth, conidial production, sclerotia formation, aflatoxin synthesis, and host colonization. Chromatin immunoprecipitation sequencing (ChIP-seq) and RNA sequencing (RNA-seq) analysis revealed that SntB played key roles in oxidative stress response of A. flavus, influencing related gene activity, especially catC encoding catalase. SntB regulated the expression activity of catC with or without oxidative stress, and was related to the expression level of the secretory lipase (G4B84_008359). The deletion of catC showed that CatC participated in the regulation of fungal morphogenesis, reactive oxygen species (ROS) level, and aflatoxin production, and that CatC significantly regulated fungal sensitive reaction and AFB1 yield under oxidative stress. Our study revealed the potential machinery that SntB regulated fungal morphogenesis, mycotoxin anabolism, and fungal virulence through the axle of from H3K36me3 modification to fungal virulence and mycotoxin biosynthesis. The results of this study shed light into the SntB-mediated transcript regulation pathways of fungal mycotoxin anabolism and virulence, which provided potential strategy to control the contamination of A. flavus and its aflatoxins.

Capsular Polysaccharide Production in Bacteria of the Mycoplasma Genus: A Huge Diversity of Pathways and Synthases for So-Called Minimal Bacteria.

Mycoplasmas are wall-less bacteria with many species spread across various animal hosts in which they can be pathogenic. Despite their reduced anabolic capacity, some mycoplasmas are known to secrete hetero- and homopolysaccharides, which play a role in host colonization through biofilm formation or immune evasion, for instance. This study explores how widespread the phenomenon of capsular homopolysaccharide secretion is within mycoplasmas, and investigates the diversity of both the molecules produced and the synthase-type glycosyltransferases responsible for their production. Fourteen strains representing 14 (sub)species from four types of hosts were tested invitro for their polysaccharide secretion using both specific (immunodetection) and nonspecific (sugar dosage) assays. We evidenced a new, atypical homopolymer of β-(1 → 6)-glucofuranose (named glucofuranan) in the human pathogen Mycoplasma (M.) fermentans, as well as a β-(1 → 6)-glucopyranose polymer for the turkey pathogen M. iowae and galactan (β-(1 → 6)-galactofuranose) and β-(1 → 2)-glucopyranose for M. bovigenitalium infecting ruminants. Sequence and phylogenetic analyses revealed a huge diversity of synthases from varied Mycoplasma species. The clustering of these membrane-embedded glycosyltransferases into three main groups was only partially correlated to the structure of the produced homopolysaccharides.

Unraveling the dynamics of Xanthomonas' flagella: insights into host-pathogen interactions.

Understanding the intricate interplay between plants and bacteria is paramount for elucidating mechanisms of immunity and disease. This review synthesizes current knowledge on the role of flagella in bacterial motility and host recognition, shedding light on the molecular mechanisms underlying plant immunity and bacterial pathogenicity. We delve into the sophisticated signaling network of plants, highlighting the pivotal role of pattern recognition receptors (PRRs) in detecting conserved molecular patterns known as microbe-associated molecular patterns (MAMPs), with a particular focus on flagellin as a key MAMP. Additionally, we explore recent discoveries of solanaceous-specific receptors, such as FLAGELLIN SENSING 3 (FLS3), and their implications for plant defense responses. Furthermore, we examine the role of bacterial motility in host colonization and infection, emphasizing the multifaceted relationship between flagella-mediated chemotaxis and bacterial virulence. Through a comprehensive analysis of flagellin polymorphisms within the genus Xanthomonas, we elucidate their potential impact on host recognition and bacterial pathogenicity, offering insights into strategies for developing disease-resistant crops. This review is intended for professionals within the fields of crops sciences and microbiology.

A master regulator of central carbon metabolism directly activates virulence gene expression in attaching and effacing pathogens.

The ability of the attaching and effacing pathogens enterohaemorrhagic Escherichia coli (EHEC) and Citrobacter rodentium to overcome colonisation resistance is reliant on a type 3 secretion system used to intimately attach to the colonic epithelium. This crucial virulence factor is encoded on a pathogenicity island known as the Locus of Enterocyte Effacement (LEE) but its expression is regulated by several core-genome encoded transcription factors. Here, we unveil that the core transcription factor PdhR, traditionally known as a regulator of central metabolism in response to cellular pyruvate levels, is a key activator of the LEE. Through genetic and molecular analyses, we demonstrate that PdhR directly binds to a specific motif within the LEE master regulatory region, thus activating type 3 secretion directly and enhancing host cell adhesion. Deletion of pdhR in EHEC significantly impacted the transcription of hundreds of genes, with pathogenesis and protein secretion emerging as the most affected functional categories. Furthermore, in vivo studies using C. rodentium, a murine model for EHEC infection, revealed that PdhR is essential for effective host colonization and maximal LEE expression within the host. Our findings provide new insights into the complex regulatory networks governing bacterial pathogenesis. This research highlights the intricate relationship between virulence and metabolic processes in attaching and effacing pathogens, demonstrating how core transcriptional regulators can be co-opted to control virulence factor expression in tandem with the cell's essential metabolic circuitry.

Membership robustness but structural change of the native gut microbiota of bumble bees upon systemic immune induction.

Our work demonstrates how innate immunity may influence the host-associated microbiota. While previous work has demonstrated the role of adaptive immunity in regulating the microbiota, we show that stimulation of an innate immune response in bumble bees may disrupt the native gut microbial community by shifting individual abundances of some members and pairwise associations. This work builds upon previous work in bumble bees demonstrating factors determining microbe colonization of hosts and microbiota membership, implicating immune response-induced changes as a factor shaping these important gut communities. While some microbiota members appear unaffected, changes in others and the community overall suggests that collateral perturbation of the native gut microbiota upon an innate immune response may serve as an additional selective pressure that shapes the evolution of host innate immunity.