Pathogen Interactions Research Articles

Transcriptomic Profiling Reveals Altered Expression of Genes Involved in Metabolic and Immune Processes in NDV-Infected Chicken Embryos

Objective: The poultry industry is significantly impacted by viral infections, particularly Newcastle Disease Virus (NDV), which leads to substantial economic losses. It is essential to comprehend how the sequence of development affects biological pathways and how early exposure to infections might affect immune responses. Methods: This study employed transcriptome analysis to investigate host–pathogen interactions by analyzing gene expression changes in NDV-infected chicken embryos’ lungs. Result: RNA-Seq reads were aligned with the chicken reference genome (Galgal7), revealing 594 differentially expressed genes: 264 upregulated and 330 downregulated. The most overexpressed genes, with logFC between 8.15 and 8.75, included C8A, FGG, PIT54, FETUB, APOC3, and FGA. Notably, downregulated genes included BPIFB3 (−4.46 logFC) and TRIM39.1 (−4.26 logFC). The analysis also identified 29 novel transcripts and 20 lncRNAs that were upregulated. Gene Ontology and KEGG pathways’ analyses revealed significant alterations in gene expression related to immune function, metabolism, cell cycle, nucleic acid processes, and mitochondrial activity due to NDV infection. Key metabolic genes, such as ALDOB (3.27 logFC), PRPS2 (2.66 logFC), and XDH (2.15 logFC), exhibited altered expression patterns, while DCK2 (−1.99 logFC) and TK1 (−2.11 logFC) were also affected. Several immune-related genes showed significant upregulation in infected lung samples, including ALB (6.15 logFC), TLR4 (1.86 logFC), TLR2 (2.79 logFC), and interleukin receptors, such as IL1R2 (3.15 logFC) and IL22RA2 (1.37 logFC). Conversely, genes such as CXCR4 (−1.49 logFC), CXCL14 (−2.57 logFC), GATA3 (−1.51 logFC), and IL17REL (−2.93 logFC) were downregulated. The higher expression of HSP genes underscores their vital role in immune responses. Conclusion: Comprehension of these genes’ interactions is essential for regulating viral replication and immune responses during infections, potentially aiding in the identification of candidate genes for poultry breed improvement amidst NDV challenges.

Biofilm formation in Streptococcus suis: in vitro impact of serovars and assessment of coinfections with other porcine respiratory disease complex bacterial pathogens

Streptococcus suis is a worldwide pathogen that impacts the swine industry, causing severe clinical signs, including meningitis and arthritis, in postweaning piglets. A key virulence mechanism of S. suis is biofilm formation, which improves its persistence and resistance to external factors. Here, we assessed the in vitro biofilm formation of 240 S. suis isolates from Spanish swine farms and evaluated the effects of serovars (SVs) and coinfections with other porcine respiratory disease complex (PRDC) pathogens. Our study revealed significant heterogeneity in biofilm formation among S. suis SVs. Notably, SV2 resulted in the lowest degree of biofilm formation, in contrast with the high biofilm-forming capacities of SV1, SV7, and SV9. Other PRDC pathogens, including Actinobacillus pleuropneumoniae, Glaesserella parasuis, and Pasteurella multocida, formed biofilms, although they were generally less robust than those of S. suis (except for SV2), which contrasts with the high biofilm formation of Staphylococcus hyicus. Coinfections enhanced biofilm formation in mixed cultures of S. suis, particularly with P. multocida. Other coinfections revealed variable results in pathogen interactions, suggesting the potential of biofilms for increased persistence and pathogenicity in coinfections. In conclusion, this study underscores the importance of serovar-specific differences in biofilm formation among S. suis isolates, with significant implications for pathogenicity and persistence. The heterogeneous biofilm formation observed in coinfections with other PRDC pathogens reveals a complex interplay that could exacerbate disease severity. These findings provide a foundation for further research on biofilm mechanisms to mitigate the impact of PRDC in the swine industry.

Unraveling the genetic basis of Rhizobium rhizogenes-mediated transformation and hairy root formation in rose using a genome-wide association study

Key MessageMultiple QTLs reveal the polygenic nature of R. rhizogenes-mediated transformation and hairy root formation in roses, with five key regions explaining 12.0–26.9% of trait variability and transformation-related candidate genes identified.Understanding genetic mechanisms of plant transformation remains crucial for biotechnology. This is particularly relevant for roses and other woody ornamentals that exhibit recalcitrant behavior in transformation procedures. Rhizobium rhizogenes-mediated transformation leading to hairy root (HR) formation provides an excellent model system to study transformation processes and host–pathogen interactions. Therefore, this study aimed to identify quantitative trait loci (QTLs) associated with HR formation and explore their relationship with adventitious root (AR) formation in rose as a model for woody ornamentals. A diversity panel of 104 in vitro grown rose genotypes was transformed with R. rhizogenes strain ATCC 15834 carrying a green fluorescent protein reporter gene. Phenotypic data on callus and root formation were collected for laminae and petioles. A genome-wide association study using 23,419 single-nucleotide polymorphism markers revealed significant QTLs on chromosomes one and two for root formation traits. Five key genomic regions explained 12.0–26.9% of trait variability, with some peaks overlapping previously reported QTLs for AR formation. This genetic overlap was supported by weak to moderate correlations between HR and AR formation traits, particularly in petioles. Candidate gene identification through literature review and transcriptomic data analysis revealed ten candidate genes involved in bacterial response, hormone signaling, and stress responses. Our findings provide new insights into the genetic control of HR formation in roses and highlight potential targets for improving transformation efficiency in ornamental crops, thereby facilitating future research and breeding applications.

Mapping of Nuclear Localization Signal in Secreted Liver-Specific Protein 2 of Plasmodium falciparum.

The secretory proteome of Plasmodium exhibits differential spatial and functional activity within host cells. Plasmodium secretes proteins that translocate into the human host cell nucleus. Liver-specific protein 2 of Plasmodium falciparum (Pf-LISP2) shows nuclear accumulation in human hepatocytes during the late liver stage of malaria parasite development. However, the nuclear translocation mechanism for Pf-LISP2 remains largely uncharacterized. Here, we identified a classical bipartite nuclear localization signal (NLS) located in the C-terminal region of Pf-LISP2. Phylogenetic analysis revealed that this NLS is unique to Plasmodium falciparum and its close relative Plasmodium reichenowi, suggesting an evolutionary adaptation linked to their shared primate hosts. Functional assays confirmed the NLS's nuclear import activity, as fusion constructs of the Pf-LISP2 NLS with Pf-aldolase (Pf-aldolase-NLS-EGFP) localized exclusively to the nucleus of HepG2 cells. Mutation analysis of key lysine and arginine residues in the bipartite NLS demonstrated that the basic amino acid clusters are essential for nuclear localization. Importin-α/β interaction was found to be crucial for Pf-LISP2 nuclear transport, as coexpression of the NLS constructs with the importin-α/β inhibitor mCherry-Bimax2 significantly blocked nuclear translocation. Specific interactions between the lysine and arginine residues of Pf-LISP2's NLS and the conserved tryptophan and asparagine residues of human importin-α1 facilitate the cytosol-to-nuclear translocation of Pf-LISP2. Additionally, LISP2 lacks any nuclear export signal. These results provide new insights into the mechanisms of nuclear transport in Plasmodium falciparum, potentially contributing to the understanding of its pathogenicity and host-cell interactions during liver-stage infection.

Multidrug and Toxic Compound Extrusion Transporters: Ubiquitous Multifaceted Proteins in Microbes, Plants, and Their Interactions

In recent years, membrane transporters have attracted considerable interest regarding their involvement in the molecular dialogue occurring between microbes and their hosts. In particular, the multidrug and toxic compound extrusion (MATE) transporters form a family of integral membrane proteins, mainly involved in the efflux of toxic and xenobiotic compounds. They are present in all living organisms, both prokaryotes and eukaryotes, where they have a wide array of extremely different roles. In plants, MATE proteins are involved in many important physiological processes, such as plant development, as well as the active transport of several secondary metabolites. In microorganisms, they are mainly implicated in the efflux of toxic compounds and thus contribute to drug resistance. Conversely, information about the actual role of MATE transporters in the interaction between plants and microorganisms, including phytopathogens, is still limited, according to the number of publications available on this topic. Indeed, an understanding of their roles in the plant–pathogen interaction could be essential to increase the knowledge of their molecular conversation and to provide data for the design and development of innovative and sustainable anti-infective strategies to control and manage plant pathogens.

Global Lipidomics Reveals the Lipid Composition Heterogeneity of Extracellular Vesicles from Drug-Resistant Leishmania

Background: The rise of drug-resistant Leishmania strains presents a significant challenge in the treatment of Leishmaniasis, a neglected tropical disease. Extracellular vesicles (EVs) produced by these parasites have gained attention for their role in drug resistance and host–pathogen interactions. Methods: This study developed and applied a novel lipidomics workflow to explore the lipid profiles of EVs from three types of drug-resistant Leishmania infatum strains compared to a wild-type strain. EVs were isolated through ultracentrifugation, and their lipid content was extracted using a modified Matyash protocol. LC-MS analysis was performed, and data processing in MS-DIAL enabled lipid identification and quantification. Statistical analysis in MetaboAnalyst revealed strain-specific lipid alterations, highlighting potential links between lipid composition and drug resistance mechanisms. Results: Our results show distinct alterations in lipid composition associated with drug resistance. Specifically, drug-resistant strains exhibited reduced levels of phosphatidylcholine (PC) and phosphatidylglycerol (PG), particularly in the amphotericin B-resistant strain LiAmB1000.1. Sterol and glycerolipid species, including cholesteryl ester (CE) and triacylglycerol (TG) were also found to be diminished in LiAmB1000.1. These changes suggest significant lipid remodeling under drug pressure, potentially altering the biophysical properties of EV membranes and their capacity for molecule transfer. Furthermore, the lipidomic profiles of EVs from the other resistant strains, LiSb2000.1 and LiMF200.5, also displayed unique alterations, underscoring strain-specific adaptations to different drug resistance mechanisms. Conclusions: These significant alterations in lipid composition suggest potential lipid-based mechanisms underlying drug resistance in Leishmania, providing new avenues for therapeutic intervention.

'Friend versus foe'-does autophagy help regulate symbiotic plant-microbe interactions and can it be manipulated to improve legume cultivation?

Autophagy is a genetically regulated, eukaryotic catabolic pathway that responds to internal and external cellular signals. In plants, it plays crucial roles in development, and responses to abiotic and biotic stresses. Due to its role in limiting the hypersensitive response, research on the molecular mechanisms of autophagic signalling pathways in plant-microbe interactions has primarily focused on plant-pathogen responses. Although there is substantially less information on the role of autophagy signalling in symbiotic plant-microbe interactions, there is accumulating evidence that it is also a key regulator of mutualistic plant-microbe interactions. Here, we review recent progress on the roles of autophagy in symbiotic plant interactions and discuss potential future research directions. Once understood, the central role that autophagy plays within pathogenic and symbiotic plant-microbe interactions has significant potential application for crop improvement. Manipulating autophagy in legume crops could help support crop growth with reduced levels of fertiliser application while maintaining yields with increased protein content in the harvest.

Transcriptome analysis of infected human macrophages between strains of Brucella melitensis and an omp31 mutant.

Brucella spp. are small aerobes non-motile Gram-negative coccobacilli that act as facultative intracellular pathogens responsible for zoonotic infections. B. melitensis can survive and replicate within host macrophages, the molecular phenomena of this host: pathogen interaction remain totally unknown. The aim of this work was to evaluate the differences in the response between human macrophages infected with different B. melitensis strains. Comparison of transcriptome data was carried out for identifying differentially expressed genes among different strain infection. We evaluated the THP-1 macrophage molecular response at early stages of infection to different strains of Brucella melitensis (B. melitensis wild- type 133 (BM133), B. melitensis ATCC 23456 (BM16M) and a B. melitensis 133 omp31 mutant (LVM31)). Our analysis revealed intriguing differences in the host cell response to two virulent strains (BM16M and BM133), infection with BM16M led to an over-expression of anti-inflammatory pathways, such as cAMP signaling and PI3K-Akt pathway, and down regulation of inflammatory pathways involving IL1A and IL10 compared to BM133. Mutant strain BMLVM31 induced an activation of the apoptotic process and the absence of Omp31, impaired the inhibition of CASP1 and CASP9 expression. Additionally, the mutation of BMLV31 impairs the evasion of cathepsin D in early stages of the infection. These findings shed light on the intricate molecular interactions between B. melitensis strains and human macrophages, providing valuable insights for understanding the pathogenesis of brucellosis.

Impact of Mycobacterium tuberculosis H37Rv Infection on Extracellular Vesicle Cargo in Macrophages: Implications for Host–Pathogen Interaction

Tuberculosis (TB) is one of the most common respiratory infections worldwide, and it is caused by Mycobacterium tuberculosis (Mtb). Mtb employs immune evasion mechanisms that allow the disease to become chronic. Despite extensive research, the host–pathogen interaction remains incompletely understood. Extracellular vesicles (EVs) are small membrane particles that play a regulatory role in infectious diseases. Host-derived EVs have been identified as carriers of proteins, messenger RNA, and lipids from both the host cells and the pathogens. In this study, we assessed the cargo of EVs in human macrophages infected with the virulent strain H37Rv of Mtb at 1 and 24 h post-infection (hpi). The results showed that 1 hpi, infected macrophages secreted EVs containing Mtb proteins (15 to 37 kDa) and Ag85 kDa, as well as RNA transcripts (ESAT-6, 5KST, Ag85, IS6110, 30 kDa, 19 kDa, and MPT64). However, these decreased at 24 hpi. The infection of macrophages with Mtb was observed to result in the release of EVs containing Ag85 protein and RNA transcripts of Mtb; this process appeared to diminish after 24 hpi, suggesting the existence of an evasion mechanism. Both Ag85 and the RNA transcripts could be potential biomarkers for the diagnosis of TB patients.

Interkingdom Communication via Extracellular Vesicles: Unraveling Plant and Pathogen Interactions and Its Potential for Next-Generation Crop Protection

Interkingdom Communication via Extracellular Vesicles: Unraveling Plant and Pathogen Interactions and Its Potential for Next-Generation Crop Protection

Host-Pathogen Interactions in Mycobacterium tuberculosis: Molecular Mechanisms and Implications for Treatment

Worldwide, tuberculosis (TB) due to Mycobacterium tuberculosis is a major public health problem with high morbidity and mortality. This review reviewed the molecular mechanisms and their implications for treatment of M. tuberculosis infection, as well as the complex host pathogen interactions underpinning M. tuberculosis infection. The ability of the pathogen to avoid the host immune responses by utilizing critical strategies for the evasion, for instance, inhibition of phagosome-lyosome fusion and modulation of the host cell pathways are discussed first. T cells play a critical role in the adaptive immune response, and granulomas develop, which are then examined in detail. It importantly informs current treatment protocols which struggle to overcome issues of patient compliance, drug resistance and toxicity. Explored are novel therapeutic approaches targeting bacterial cell wall synthesis, virulence factors and the use of host directed therapies. Recent advances in the development of vaccines, including the innovative endeavors that hope to improve or replace the BCG vaccine, are also reviewed. The review ends by anticipating future directions in TB management, which could be facilitated through efforts related to personalized medicine, and combination therapies, as well as rapid diagnostics to change how we think about treatment. The insights from this study are important for developing novel strategies to fight TB and to bring down its burden globally.

The Expression and Sequence Analysis of MdMATE52 in Apple Roots During Activation of Defense Against Pythium ultimum Infection

To understand the molecular regulation of host defense responses in the pathosystem between apple roots and a necrotrophic oomycete pathogen Pythium ultimum, a series of transcriptome analyses have revealed a multi-phase and multi-layer defense tactic in apple root tissues. Among the most notable transcriptome changes during defense activation in apple roots, upregulation of genes involved in phenylpropanoid biosynthesis, transport of secondary metabolites, and lignin formation appeared to be the key defense themes which may crucially impact the outcome of plant–pathogen interactions. From our transcriptome datasets, the MdMATE52 gene, which encodes a MATE transporter, was shown to be differentially expressed between a resistant and a susceptible apple rootstock genotype in response to P. ultimum infection. The cis elements at promoter regions and sequence variations within coding regions of MdMATE52 were compared among several resistant and susceptible apple rootstock genotypes as well as various Malus species. The stronger upregulated expression patterns of MdMATE52 appeared to be correlated with the observed resistance traits among various genotypes. Our results suggested that minimal but clearly identifiable sequence variations may contribute to the genotype-specific expression and function of MdMATE52. The findings from this study should facilitate future experiments such as site-specific mutation and Crispr-based genome editing to define the regulation mechanisms of MdMATE52 and function during defense activation in apple roots.

Ectopic expression of the grape hexose transporter VvHT5 restores STP13‐deficiency in Arabidopsis and promotes fungal resistance to Botrytis cinerea

AbstractSugar transporters play a crucial role in plant responses to environmental factors. During plant–pathogen interactions, it is well established that sugar transporters and cell wall invertases are essential for regulating sugar availability at the plant–pathogen interface, impacting both plant resistance and pathogen proliferation. Despite these insights, their role in grapevine defence against pathogens remains underexplored. We examined the expression of sugar transporter and invertase genes in grape leaves infected with the necrotrophic fungus Botrytis cinerea. Our results highlighted significant coordinated upregulation of VvHT5, VvcwINV and defence genes, suggesting a role in enhancing sink strength in infected leaves and implementing host defences. Heterologous expression of GFP‐fused proteins confirmed VvHT5 as a plasma membrane‐localized hexose symporter and phylogenetic analysis indicated its close relation with STP13‐like proteins, which are known to be implicated in host resistance across several plant–pathogen interactions. VvHT5 was heterologously expressed in Arabidopsis thaliana, resulting in high constitutive expression of the VvHT5 protein and increased glucose uptake activity. Phenotypic analysis revealed that VvHT5 enhanced basal resistance to B. cinerea and rescued the wild‐type phenotype in STP13‐deficient plants, indicating that VvHT5 is the grapevine orthologue of AtSTP13. Our findings suggest that VvHT5 may facilitate the reabsorption of extracellular monosaccharides, released from VvcwINV activity or damaged tissues during infection. This activity allows host cells to compete with necrotrophic pathogens for extracellular hexoses, thereby restricting sugar availability to the fungus. It would also support host metabolic demands for defence or serve as a signalling mechanism to orchestrate intracellular processes.

Pattern Recognition Receptors in Periodontal Disease: Molecular Mechanisms, Signaling Pathways, and Therapeutic Implications

Periodontal disease remains a significant global health concern, characterized by complex host–pathogen interactions leading to tissue destruction. This review explored the role of pattern recognition receptors (PRRs) in the pathogenesis of periodontal disease, synthesizing current knowledge on their molecular mechanisms and potential as therapeutic targets. We examined the diverse family of PRRs, focusing on toll-like receptors (TLRs) and NOD-like receptors (NLRs), elucidating their activation by periodontal pathogens and subsequent downstream signaling cascades. This review highlights the intricate interplay between PRR-mediated pathways, including NF-κB and MAPK signaling, and their impact on inflammatory responses and bone metabolism in periodontal tissues. We discussed the emerging concept of PRR crosstalk and its implications for periodontal homeostasis and disease progression. Furthermore, this review addressed the potential of PRR-targeted therapies, exploring both challenges and opportunities in translating molecular insights into clinical applications. By providing an overview of PRRs in periodontal health and disease, this review aims to stimulate future research directions and inform the development of novel diagnostic and therapeutic strategies in periodontology.

Bacterial Secondary Metabolites Embedded in Producer Cell Membranes and Antibiotics Targeting Their Biosynthesis.

The bacterial cell membrane primarily houses lipids, carbohydrates, and proteins forming a barrier and interface that maintains cellular integrity, supports homeostasis, and senses environmental changes. Compared to lipid components and excreted secondary metabolites, compounds embedded in the producer cell membrane are often overlooked due to their low abundance and niche-specific functions. The accumulation of findings has led to an increased appreciation of their crucial roles in bacterial cell biochemistry, physiology, and ecology, as well as their impact on mutualistic and pathogenic bacteria-eukaryote interactions. This review highlights the structures, biosynthesis, regulation, and ecological functions of membrane-embedded secondary metabolites. It also discusses antibiotics that target their biosynthetic pathways, aiming to inspire the development of antibiotics specific to pathogenic bacteria without harming human cells.

Unveiling the role of long non-coding RNAs in chicken immune response to highly pathogenic avian influenza H5N1 infection

Avian influenza viruses (AIVs) pose a significant threat to global poultry production, necessitating effective control strategies to mitigate economic losses and ensure animal welfare. Long non-coding RNAs (lncRNAs) have emerged as crucial regulators of immune responses, yet their roles in AIV-infected chickens remain poorly understood. This study aimed to investigate the expression profiles of lncRNAs and their targets in Vietnamese Ri chickens infected with the highly pathogenic AIV (HPAIV) H5N1. Through RNA sequencing, we identified novel lncRNAs and analyzed differentially expressed (DE) transcripts at 1 and 3 days post-infection (dpi) in chicken lung tissue. Our results revealed a higher number of DE lncRNAs and mRNAs at 1 dpi and 3 dpi, respectively, compared to control, with resistant chickens exhibiting a notably stronger immune response than susceptible chickens at 3 dpi. Functional analysis implicated these lncRNAs in immune-related pathways crucial for host responses to H5N1 viral infection. Furthermore, we identified lncRNA–mRNA interactions associated with antiviral responses and immune function. Notably, several genes involved in antiviral resistance and immune responses showed higher expression in resistant chickens, confirming their stronger antiviral response. Overall, our study provides insights into the role of lncRNAs in the host's response to HPAIV H5N1 infection in chickens and highlights potential candidates for further investigation into host–pathogen interactions. These findings could drive the development of novel control strategies for AIVs, significantly enhancing poultry health and biosecurity.

Broad-scale phenotyping in Arabidopsis reveals varied involvement of RNA interference across diverse plant-microbe interactions.

RNA interference (RNAi) is a crucial mechanism in immunity against infectious microbes through the action of DICER-LIKE (DCL) and ARGONAUTE (AGO) proteins. In the case of the taxonomically diverse fungal pathogen Botrytis cinerea and the oomycete Hyaloperonospora arabidopsidis, plant DCL and AGO proteins have proven roles as negative regulators of immunity, suggesting functional specialization of these proteins. To address this aspect in a broader taxonomic context, we characterized the colonization pattern of an informative set of DCL and AGO loss-of-function mutants in Arabidopsis thaliana upon infection with a panel of pathogenic microbes with different lifestyles, and a fungal mutualist. Our results revealed that, depending on the interacting pathogen, AGO1 acts as a positive or negative regulator of immunity, while AGO4 functions as a positive regulator. Additionally, AGO2 and AGO10 positively modulated the colonization by a fungal mutualist. Therefore, analyzing the role of RNAi across a broader range of plant-microbe interactions has identified previously unknown functions for AGO proteins. For some pathogen interactions, however, all tested mutants exhibited wild-type-like infection phenotypes, suggesting that the roles of AGO and DCL proteins in these interactions may be more complex to elucidate.

Effector-Mediated Suppression of Programmed Cell Death by Phytophthora palmivora in Oil Palm.

Phytophthora palmivora is the pathogen causing bud rot in oil palm (Elaeis guineensis). This pathogen secretes effector proteins that manipulate host defenses, contributing to disease progression. In this study, we systematically investigated the role of specific effector proteins in suppressing programmed cell death (PCD) in oil palm leaflets. Our approach included using genomic and transcriptomic data from a Colombian P. palmivora isolate alongside the coexpression network of a substantial effector dataset. From this analysis, ten candidate effectors were selected, characterized, and evaluated for their ability to suppress PCD in oil palm leaflets through transient expression via biolistics. Several effectors exhibited significant anti-PCD activity in susceptible and less susceptible oil palm genotypes. Notably, the effectors Avr3F (689), RxLR (1540), and RxLR (1546) demonstrated suppression of PCD in both genotypes, while the other effectors played variable roles in PCD regulation. Phylogenetic analysis further identified distinct clades among the effectors, possibly associated with their functional activities. Additionally, specific motifs, such as RXLR-dEER, K, and Y, appeared to correlate with PCD suppression. This research enhances our understanding of the molecular mechanisms underlying the interaction between P. palmivora effectors and oil palm host responses, highlighting these proteins' genotype-specific regulation of PCD. The findings contribute valuable insights into plant-pathogen interactions and offer potential avenues for targeted disease control strategies in the oil palm industry.

Cold snaps lead to a 5-fold increase or a 3-fold decrease in disease proliferation depending on the baseline temperature

BackgroundClimate change is driving increased extreme weather events that can impact ecology by moderating host–pathogen interactions. To date, few studies have explored how cold snaps affect disease prevalence and proliferation. Using the Daphnia magna–Ordospora colligata host-parasite system, a popular model system for environmentally transmitted diseases, the amplitude and duration of cold snaps were manipulated at four baseline temperatures, 10 days post-exposure, with O. colligata fitness recorded at the individual level.ResultsCold snaps induced a fivefold increase or a threefold decrease in parasite burden relative to baseline temperature, with complex nuances and varied outcomes resulting from different treatment combinations. Both amplitude and duration can interact with the baseline temperature highlighting the complexity and baseline dependence of cold snaps. Furthermore, parasite fitness, i.e., infection prevalence and burden, were simultaneously altered in opposite directions in the same cold snap treatment.ConclusionsWe found that cold snaps can yield complicated outcomes that are unique from other types of temperature variation (for example, heatwaves). These results underpin the challenges and complexity in understanding and predicting how climate and extreme weather may alter disease under global change.

Strategic genetic insights and integrated approaches for successful management of blackleg in canola/rapeseed farming

AbstractThis review describes a triumphant narrative in the battle against the devastating plant pathogen complex, Leptosphaeria maculans and L. biglobosa, and the success of the world's second‐largest oilseed crop, canola/oilseed rape. Emphasizing global collaborations, the article explores successfully mitigating this destructive disease in canola/rapeseed production across Australia, Canada and Europe. It highlights how strategies may vary between continents to adapt to specific contexts. While initial resistance (R) genes proved effective, the evolution of the pathogen under crop‐induced disease pressure led to the breakdown of these genes. Now, growers in these regions have been equipped with new tools, allowing them to make informed decisions that help to keep the disease at generally low levels. A pivotal factor in this success has been a deepened understanding of the intricate science underlying the host–pathogen interaction. Concerted efforts of individual laboratories and collaborative initiatives have played an essential role in this success, including novel methods for disease control based on extensive research that has translated into developing highly resistant varieties, enhanced pathogen monitoring, improved cultivar recommendation and integrated management strategies. The review showcases many milestone advancements, including the cloning of numerous avirulence genes within the pathogen, characterization of specific R genes, the development of various molecular tools for monitoring both pathogen and host, the introduction of groundbreaking disease management strategies such as R gene labelling, rotation and stacking, and establishment of a universal pathogen isolate collection that facilitates the exchange of information among multiple laboratories and adds a new dimension to this triumph.