Biology subjects

McDonald, B.

Publications and source records attributed to McDonald, B..

18 recordsLinked to original sources

bioRxiv2026

Wildlife feeding increases risk of male wild turkeys (Meleagris gallopavo) to hunter harvest

Wildlife feeding during the wild turkey (Meleagris gallopavo) hunting season is legal in many states within the United States, but hunting turkeys with the aid of bait is unlawful in most states. The most common policy to prevent wildlife feeding from acting as bait is to restrict hunting within a defined radius. However, the effect of wildlife feeders on turkey harvest risk and the effectiveness of distance restrictions on mitigating that influence have not been investigated. During 2024-2025, we used GPS transmitters to track 30 adult male turkeys during the spring hunting season on private land with active feeders in Florida, USA, where hunting turkeys within a 91 m radius of a feeder was unlawful. We used Cox proportional hazard models to link risk of hunter harvest with unique feeders visited daily, number of feeders within a home range, and average morning distance and roosting distance to feeders at multiple temporal scales. Hunters harvested 53% of the tagged turkeys. Risk of hunter harvest increased with the number of unique feeders visited the previous day and after the first three days of hunting season with the number of active feeders within a home range. As distance from the most recent roost site and average morning distance to a feeder decreased, risk of hunter harvest increased. We estimated that risk of hunter harvest would be reduced by over 50% if distance restrictions were increased from 100 m to 200 m, by nearly 75% with an increase from 100 m to 300 m, and by nearly 90% with an increase from 100 m to 500 m. To completely eliminate the influence of wildlife feeders on risk of hunter harvest would require a restriction distance well beyond a 500m radius, which is impractical given that this radius would result in an area twice the average private landowner property size in the region. Thus, if wildlife feeding during the turkey hunting season is to be allowed, it will act as bait, in which case, the acceptable level of its influence as bait can be achieved with the appropriate hunting radius restriction.

ecology↗

bioRxiv2026

Early sex-specific organ transcriptional divergence without physiological differences in a murine model of fecal-induced peritonitis

Sepsis is defined as a dysregulated response to infection, leading to life-threatening organ dysfunction that particularly affects parenchymal organs. Clinical studies remain inconclusive regarding the impact of biological sex on sepsis, and preclinical studies are predominantly performed in male animals. We examined early (8 h) septic responses in male and female mice using a fecal-induced peritonitis (FIP) model. Blood biochemical parameters, body temperature, and murine sepsis scores provided evidence of a septic response in animals randomized to FIP compared to controls, but showed no physiological differences between male and female mice. Transcriptomic analysis of the liver, kidney, and lung showed consistent inflammatory activation in response to sepsis as compared to controls. Notably, in the kidney and lung, female mice exhibited stronger immune activation and a heightened inflammatory response compared to males. Thus, biological sex differences in the septic response can be detected in early acute sepsis without apparent physiological differences.

pathology↗

bioRxiv2025

Differential disease tolerance mediates sex-biased illness severity in sepsis

Sepsis in humans, as well as mouse models of infection, demonstrates sex-biased outcomes in which males tend to have a higher incidence, higher severity, and higher mortality compared to females. Despite this important sex-bias in sepsis outcomes, little is known about its mechanistic drivers nor therapeutic implications, as much of the foundational data on sepsis pathogenesis is derived from animal studies that included only male subjects, potentially contributing to the notable paucity of successful mouse-to-human translation of sepsis therapeutics. In this study, we demonstrate that male-biased illness severity and organ dysfunction in mouse models of bacterial sepsis is mediated by impaired disease tolerance in males, involving impaired tolerogenic shifts in mitochondrial oxidative metabolism compared to females. Microbiological analyses and systems immunology characterization of sepsis between males and females revealed that sex-biased disease tolerance was independent of infection resistance mechanisms, as well as canonical immune/inflammatory dysregulation. Therapeutic potentiation of mitochondrial tolerance with doxycycline neutralized sexual dimorphism of illness severity and organ dysfunction through a male-predominant treatment effect. These data reveal that biological sex is a fundamental determinant of illness severity and treatment-responsiveness in sepsis through modulation of disease tolerance, which may be harnessed therapeutically to address sex-biased outcomes in sepsis. One sentence summarySex-biased illness severity in bacterial sepsis is caused by impaired disease tolerance in males that can be rescued by therapeutic potentiation of mitochondrial tolerance

pathology↗

bioRxiv2024

Different signaling interpretations by PKC eta and theta control T cell function and exhaustion

Chronic antigen signaling drives CD8+ T cell exhaustion (TEX) in cancer and chronic infection. However, how the kinase cascades downstream of the T cell receptor drive exhaustion is not understood. We found that continuous agonism of protein kinase C (PKC) causes degradation of PKC theta, but not PKC eta, and induces terminal TEX cells. During chronic infection, PKC theta is necessary to maintain the progenitor exhausted (TEX-PROG) cells, and thus the antigen-specific T cell response, while agonism of PKC eta promotes terminal exhaustion (TEX-TERM) in vitro and in vivo. The cascades downstream of these kinases are distinct, with PKC theta promoting activity of canonical PKC targets in the MAPK and CDK families, while eta promotes activity of other targets, including casein kinase I G2 (CK1G2). Expression of an engineered, degradation-resistant PKC theta, or deletion of the gene encoding CK1G2, improves T cell function and tumor control. Our illustration of multiple therapeutic avenues arising from targeting PKC highlights its centrality in TEX differentiation and its clinical potential in cancer immunotherapy. HighlightsO_LIPKC theta sustains T cell function while PKC eta promotes terminal exhaustion C_LIO_LIPKC theta and eta drive distinct phospho-cascades to oppose each others differentiation instructions C_LIO_LIAn engineered, degradation-resistant PKC theta improves T cell responses in chronic infection and cancer C_LIO_LIAblation of kinase CK1G2 downstream of PKC eta improves anti-tumor T cell responses C_LI

immunology↗

bioRxiv2024

Diverse somatic Transformer and sex chromosome karyotype pathways regulate gene expression in Drosophila gonad development

The somatic sex determination gene transformer (tra) is required for the highly sexually dimorphic development of most somatic cells, including those of the gonads. In addition, somatic tra is required for the germline development even though it is not required for sex determination within germ cells. Germ cell autonomous gene expression is also necessary for their sex determination. To understand the interplay between these signals, we compared the phenotype and gene expression of larval wild-type gonads and the sex-transformed tra gonads. XX larval ovaries transformed into testes were dramatically smaller than wild-type, with significant reductions in germ cell number, likely due to altered geometry of the stem cell niche. Additionally, there was a defect in progression into spermatocyte stages. XY larval testes transformed into ovaries had excessive germ cells, possibly due to the earlier onset of cell division. We suggest that germ cells are neither fully female nor male following somatic sex transformation, with certain pathways characteristic of each sex expressed in tra mutants. We found multiple patterns of somatic and germline gene expression control exclusively due to tra, exclusively due to sex chromosome karyotype, but usually due to a combination of these factors showing tra and sex chromosome karyotype pathways regulate gene expression during Drosophila gonad development.

developmental biology↗

bioRxiv2023

Genome-wide association studies reveal a rapidly evolving candidate avirulence effector in the Cercospora leaf spot pathogen Cercospora beticola

The major resistance gene BvCR4 recently bred into sugar beets provides a high level of resistance to Cercospora leaf spot caused by the fungal pathogen Cercospora beticola. The occurrence of pathogen strains virulent to BvCR4 was studied using field trials in Switzerland. Virulence of a subset of these strains was evaluated in a field trial conducted under elevated artificial disease pressure. We created a new C. bet cola reference genome and mapped whole genome sequences of 256 field-collected isolates. These were combined with virulence phenotypes to conduct three separate GWAS to identify candidate avirulence genes. We identified a locus associated with avirulence containing a single candidate avirulence effector gene named AvrCR4. All virulent isolates either lacked AvrCR4 or had non-synonymous mutations within the gene. AvrCR4 was present in all 74 isolates from non-BvCR4 hybrids, whereas 33 of 89 isolates from BvCR4 hybrids carried a deletion. We also mapped genomic data from 190 publicly available U.S. isolates to our new reference genome. The AvrCR4 deletion was found in only one of 95 unique isolates from non-BvCR4 hybrids in the U.S. AvrCR4 presents a unique example of an avirulence effector in which virulent alleles have only recently emerged. Most likely these were selected out of standing genetic variation after deployment of BvCR4. Identification of AvrCR4 will enable real-time screening of C. beticola populations for the emergence and spread of virulent isolates.

evolutionary biology↗

bioRxiv2023

Combining high-resolution imaging, deep learning, and dynamic modelling to separate disease and senescence in wheat canopies

Maintenance of sufficient healthy green leaf area after anthesis is key to ensuring an adequate assimilate supply for grain filling. Tightly regulated age-related physiological senescence and various biotic and abiotic stressors drive overall greenness decay dynamics under field conditions. Besides direct effects on green leaf area in terms of leaf damage, stressors often anticipate or accelerate physiological senescence, which may multiply their negative impact on grain filling. Here, we present an image processing methodology that enables the monitoring of chlorosis and necrosis separately for ears and shoots (stems + leaves) based on deep learning models for semantic segmentation and color properties of vegetation. A vegetation segmentation model was trained using semi-synthetic training data generated using image composition and generative adversarial neural networks, which greatly reduced the risk of annotation uncertainties and annotation effort. Application of the models to image time-series revealed temporal patterns of greenness decay as well as the relative contributions of chlorosis and necrosis. Image-based estimation of greenness decay dynamics was highly correlated with scoring-based estimations (r {approx} 0.9). Contrasting patterns were observed for plots with different levels of foliar diseases, particularly septoria tritici blotch. Our results suggest that tracking the chlorotic and necrotic fractions separately may enable (i) a separate quantification of the contribution of biotic stress and physiological senescence on overall green leaf area dynamics and (ii) investigation of the elusive interaction between biotic stress and physiological senescence. The potentially high-throughput nature of our methodology paves the way to conducting genetic studies of disease resistance and tolerance.

plant biology↗

bioRxiv2022

Multi-drug resistant E. coli displace commensal E. coli from the intestinal tract, a trait associated with elevated levels of genetic diversity in carbohydrate metabolism genes.

Extra-intestinal pathogenic E. coli (ExPEC) can cause a variety of infections outside of the intestine and are a major causative agent of urinary tract infections. Treatment of these infections is increasingly frustrated by antimicrobial resistance (AMR) diminishing the number of effective therapies available to clinicians. Incidence of multi-drug resistance (MDR) is not uniform across the phylogenetic spectrum of E. coli. Instead AMR is concentrated in select lineages, such as ST131, which are MDR pandemic clones that have spread AMR globally. Using a gnotobiotic mouse model we demonstrate that an MDR E. coli ST131 is capable out-competing and displacing non-MDR E. coli from the gut in vivo. This is achieved in the absence of antibiotic treatment mediating a selective advantage. In mice colonised with non-MDR E. coli strains, challenge with MDR E. coli either by oral gavage or co-housing with MDR E. coli colonized mice results in displacement and dominant intestinal colonization by MDR E. coli ST131. To investigate the genetic basis of this superior gut colonization ability by MDR E. coli, we used a functional pangenomic analysis of 19,571 E. coli genomes revealing that carriage of AMR genes is associated with increased diversity in carbohydrate metabolism genes. The data presented here demonstrate that independent of antibiotic selective pressures, MDR E. coli display a competitive advantage to colonise the mammalian gut and points to a vital role of metabolism in the evolution and success of MDR lineages of E. coli via carriage and spread.

microbiology↗

bioRxiv2022

A microglia-CD4+ T cell partnership generates protective anti-tumor immunity to glioblastoma

The limited efficacy of immunotherapies against glioblastoma illustrates the urgent need to better understand the interactions between the central nervous system and the immune system. Here, we showed that a protective response to CTLA-4 therapy depended on a mutualistic relationship between microglia and CD4+ T cells. Suppression of gliomas by CD4+ T cells did not require tumor-intrinsic MHC-II expression, but rather was dependent on the selective expression of MHC-II and antigen presentation by local microglia that in turn, sustained CD4+ T cell tumoricidal effector functions. CD4+ T cell secretion of IFN{gamma} made the glioma cells vulnerable to enhanced tumor surveillance and phagocytosis by microglia via the AXL/MER tyrosine kinase receptors that were necessary for tumor suppression. This work illustrates a novel partnership between CD4+ T cells and microglia that unleashes the tumoricidal properties of microglia that can be harnessed to improve immunotherapies for glioblastoma.

immunology↗

bioRxiv2022

Genetic mapping of multiple metabolic traits identifies novel genes for adiposity, lipids and insulin secretory capacity in outbred rats

Despite the successes of human genome-wide association studies, the causal genes underlying most metabolic traits remain unclear. We used outbred heterogeneous stock (HS) rats, coupled with expression data and mediation analysis, to identify quantitative trait loci (QTLs) and candidate gene mediators for adiposity, glucose tolerance, serum lipids and other metabolic traits. Physiological traits were measured in 1519 male HS rats, with liver and adipose transcriptomes measured in over 410 rats. Genotypes were imputed from low coverage whole genome sequence. Linear mixed models were used to detect physiological and expression QTLs (pQTLs and eQTLs, respectively), employing both SNP- and haplotype-based models for pQTL mapping. Genes with cis-eQTLs that overlapped pQTLs were assessed as causal candidates through mediation analysis. We identified 15 SNP-based pQTLs and 19 haplotype-based pQTLs, of which 11 were in common. Using mediation, we identified the following genes as candidate mediators of pQTLs: Grk5 for a fat pad weight pQTL on Chr1, Krtcap3 for fat pad weight and serum lipids pQTLs on Chr6, Ilrun for a fat pad weight pQTL on Chr20 and Rfx6 for a whole pancreatic insulin content pQTL on Chr20. Furthermore, we verified Grk5 and Ktrcap3 using gene knock-down/out models, thereby shedding light on novel regulators of obesity.

genetics↗

bioRxiv2021

SMAD4 and TGFβ are architects of inverse genetic programs during fate-determination of antiviral memory CD8 T cells

Transforming growth factor {beta} (TGF{beta}) is a morphogenic protein that augments antiviral immunity by altering the functional properties of pathogen-specific memory CD8 T cells. During infection TGF{beta} inhibits formation of effector (TEFF) and central memory CD8 T cells (TCM), while encouraging tissue-resident memory CD8 T cells (TRM) to settle in peripheral tissues. SMAD proteins are signaling intermediates that are used by members of the TGF cytokine family to modify gene expression. For this study, RNA-sequencing was used to explore how regulation via SMAD4 alters the transcriptional profile of antiviral CTLs during infection. We show that SMAD4 and TGF{beta} cooperatively regulate a collection of genes that determine whether specialized populations of pathogen-specific CTLs circulate around the body, or settle in peripheral tissue. The target genes include multiple homing receptors (CD103, KLRG1 and CD62L) and transcription factors (Hobit and EOMES) that support memory formation. While TGF{beta} uses a canonical SMAD-dependent signaling pathway to induce CD103 expression on TRM cells, an alternative SMAD4-dependent mechanism is required for formation of TEFF and TCM cells in the circulation. Graphical abstractTGF{beta} and SMAD4 modulate gene expression in reciprocal directions during differentiation of antiviral CTLs. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=132 SRC="FIGDIR/small/472993v2_ufig1.gif" ALT="Figure 1"> View larger version (36K): org.highwire.dtl.DTLVardef@5ac140org.highwire.dtl.DTLVardef@455a2aorg.highwire.dtl.DTLVardef@1227d96org.highwire.dtl.DTLVardef@16336b9_HPS_FORMAT_FIGEXP M_FIG C_FIG

immunology↗

bioRxiv2021

An Immune Cell Atlas Reveals Dynamic COVID-19 Specific Neutrophil Programming Amendable to Dexamethasone Therapy

SARS-CoV-2 is a novel coronavirus that causes acute respiratory distress syndrome (ARDS), death and long-term sequelae. Innate immune cells are critical for host defense but are also the primary drivers of ARDS. The relationships between innate cellular responses in ARDS resulting from COVID-19 compared to other causes of ARDS, such as bacterial sepsis is unclear. Moreover, the beneficial effects of dexamethasone therapy during severe COVID-19 remain speculative, but understanding the mechanistic effects could improve evidence-based therapeutic interventions. To interrogate these relationships, we developed an scRNA-Seq and plasma proteomics atlas (biernaskielab.ca/COVID_neutrophil). We discovered that compared to bacterial ARDS, COVID-19 was associated with distinct neutrophil polarization characterized by either interferon (IFN) or prostaglandin (PG) active states. Neutrophils from bacterial ARDS had higher expression of antibacterial molecules such as PLAC8 and CD83. Dexamethasone therapy in COVID patients rapidly altered the IFNactive state, downregulated interferon responsive genes, and activated IL1R2+ve neutrophils. Dexamethasone also induced the emergence of immature neutrophils expressing immunosuppressive molecules ARG1 and ANXA1, which were not present in healthy controls. Moreover, dexamethasone remodeled global cellular interactions by changing neutrophils from information receivers into information providers. Importantly, male patients had higher proportions of IFNactive neutrophils, a greater degree of steroid-induced immature neutrophil expansion, and increased mortality benefit compared to females in the dexamethasone era. Indeed, the highest proportion of IFNactive neutrophils was associated with mortality. These results define neutrophil states unique to COVID-19 when contextualized to other life-threatening infections, thereby enhancing the relevance of our findings at the bedside. Furthermore, the molecular benefits of dexamethasone therapy are also defined, and the identified pathways and plasma proteins can now be targeted to develop improved therapeutics.

immunology↗

bioRxiv2020

Oxidized Lipids and CD36-Mediated Lipid Peroxidation in CD8 T Cells Suppress Anti-Tumor Immune Responses

T cell metabolic fitness plays a pivotal role in anti-tumor immunity and metabolic deregulation causes T cell dysfunction (i.e., exhaustion) in cancer. We identify that the scavenger receptor CD36 limits anti-tumor CD8+ T cell effector functions through lipid peroxidation. In murine tumors, oxidized phospholipids (OxPLs) were highly abundant and CD8+ TILs increased uptake and accumulation of lipids and lipid peroxidation. Functionally exhausted CD8+ TILs substantially increased CD36 expression and CD36-deficient CD8+ TILs had more robust anti-tumor activity and cytokine production than wild-type cells. We further show that CD36 promotes uptake of oxidized low-density lipoproteins (OxLDL) and induces lipid peroxidation in CD8+ TILs, and OxLDL inhibits CD8+ T cell functions in a CD36-dependent manner. Moreover, glutathione peroxidase 4 (GPX4) over-expression lowers lipid peroxidation and restores functionalities in CD8+ TILs. These results define a key role for an oxidized lipid-CD36 axis in promoting intratumoral CD8+ T cell dysfunction.

immunology↗

bioRxiv2020

USH2A is a Meissner corpuscle end-organ protein necessary for vibration sensing in mice and humans

Fingertip mechanoreceptors comprise sensory neuron endings together with specialized skin cells that form the end-organ. Exquisitely sensitive vibration-sensing neurons are associated with Meissners corpuscles and Pacinian corpuscles1. Such end-organ structures have been recognized for more than 160 years, but their exact functions have remained a matter of speculation. Here we examined the role of USH2A in touch sensation in humans and mice. The USH2A gene encodes a transmembrane protein with a very large extracellular domain. Pathogenic USH2A mutations cause Usher syndrome associated with hearing loss and visual impairment2. We show that patients with biallelic pathogenic USH2A mutations also have profound impairments in vibrotactile touch perception. Similarly, mice lacking the USH2A protein showed severe deficits in a forepaw vibrotactile discrimination task. Forepaw rapidly-adapting mechanoreceptors (RAMs) recorded from Ush2a-/- mice innervating Meissners corpuscles showed profound reductions in their vibration sensitivity. However, the USH2A protein was not expressed in sensory neurons, but was found in specialized terminal Schwann cells in Meissners corpuscles. Loss of this large extracellular tether-like protein in corpuscular end-organs innervated by RAMs was sufficient to reduce the vibration sensitivity of mechanoreceptors. Thus, USH2A expressed in corpuscular end-organs associated with vibration sensing is required to properly perceive vibration. We propose that cells within the corpuscle present a tether-like protein that may link to mechanosensitive channels in sensory endings to facilitate small amplitude vibration detection essential for the perception of fine textured surfaces.

neuroscience↗

bioRxiv2020

Functional delineation of tissue-resident CD8 T cell heterogeneity during infection and cancer

Unremitting defense against diverse pathogens and malignancies requires a dynamic and durable immune response. Tissue-resident memory CD8+ T cells (TO_SCPLOWRMC_SCPLOW) afford robust protection against infection and cancer progression through continuous surveillance of non-lymphoid tissues. Here, we provide insight into how TO_SCPLOWRMC_SCPLOW confer potent and persistent immunity through partitioning of distinct cellular subsets differing in longevity, effector function, and multipotency. Antigen-specific CD8+ T cells localized to the epithelium of the small intestine are primarily comprised of a shorter-lived effector population most prominent early following both acute viral and bacterial infections, and a longer-lived Id3hi TO_SCPLOWRMC_SCPLOW population that subsequently accumulates at later memory timepoints. We define regulatory gene-programs driving these distinct TO_SCPLOWRMC_SCPLOW states, and further clarify roles for Blimp1, T-bet, Id2, and Id3 in supporting and maintaining intestinal TO_SCPLOWRMC_SCPLOW heterogeneity during infection. Further, through single-cell RNAseq analysis we demonstrate that tumor-infiltrating lymphocytes broadly differentiate into discrete populations of short-lived and long-lived TO_SCPLOWRMC_SCPLOW-like subsets, which share qualities with terminally-exhausted and progenitor-exhausted cells, respectively. As the clinical relevance of TO_SCPLOWRMC_SCPLOW continues to widen from acute infections to settings of chronic inflammation and malignancy, clarification of the spectrum of phenotypic and functional states exhibited by CD8+ T cells that reside in non-lymphoid tissues will provide a framework for understanding their regulation and identity in diverse pathophysiological contexts.

immunology↗

bioRxiv2019

Natural selection drives population divergence for local adaptation in a wheat pathogen

Evolution favors the emergence of locally-adapted optimum phenotypes that are likely to differ across a wide array of environmental conditions. The emergence of favorable adaptive characteristics is accelerated in agricultural pathogens due to the unique properties of agro-ecosystems. We performed a QST - FST comparison using 164 strains of Parastagonospora nodorum sampled from eight global field populations to disentangle the predominant evolutionary forces driving population divergence in a wheat pathogen. We used digital image analysis to obtain quantitative measurements of growth rate and melanization at different temperatures and under different fungicide concentrations in a common garden experiment. FST measures were based on complete genome sequences obtained for all 164 isolates. Our analyses indicated that all measured traits were under selection. Growth rates at 18{degrees}C and 24{degrees}C were under stabilizing selection (QST < FST), while diversifying selection (QST > FST) was the predominant evolutionary force affecting growth under fungicide and high temperature stress. Stabilizing selection (QST < FST) was the predominant force affecting melanization across the different environments. Melanin production increased at 30{degrees}C but was negatively correlated with higher growth rates, consistent with a trade-off under heat stress. Our results demonstrate that global populations of P. nodorum possess significant evolutionary potential to adapt to changing local conditions, including warmer temperatures and applications of fungicides.

evolutionary biology↗

bioRxiv2018

Precision phenotyping reveals novel loci for quantitative resistance to septoria tritici blotch in European winter wheat

O_LIAccurate, high-throughput phenotyping for quantitative traits is the limiting factor for progress in plant breeding. We developed automated image analysis to measure quantitative resistance to septoria tritici blotch (STB), a globally important wheat disease, enabling identification of small chromosome intervals containing plausible candidate genes for STB resistance.\nC_LIO_LI335 winter wheat cultivars were included in a replicated field experiment that experienced natural epidemic development by a highly diverse but fungicide-resistant pathogen population. More than 5.4 million automatically generated phenotypes were associated with 13,648 SNP markers to perform a GWAS.\nC_LIO_LIWe identified 26 chromosome intervals explaining 1.9-10.6% of the variance associated with four resistance traits. Seventeen of the intervals were less than 5 Mbp in size and encoded only 173 genes, including many genes associated with disease resistance. Five intervals contained four or fewer genes, providing high priority targets for functional validation. Ten chromosome intervals were not previously associated with STB resistance.\nC_LIO_LIOur experiment illustrates how high-throughput automated phenotyping can accelerate breeding for quantitative disease resistance. The SNP markers associated with these chromosome intervals can be used to recombine different forms of quantitative STB resistance that are likely to be more durable than pyramids of major resistance genes.\nC_LI

plant biology↗

bioRxiv2017

The wheat blast pathogen Pyricularia graminis-tritici has complex origins and a disease cycle spanning multiple grass hosts

The wheat blast disease has been a serious constraint for wheat production in Latin America since the late 1980s. We used a population genomics analysis including 95 genome sequences of the wheat blast pathogen Pyricularia graminis-tritici (Pygt) and other Pyricularia species to show that Pygt is a distinct, highly diverse pathogen species with a broad host range. We assayed 11 neutral SSR loci in 526 Pygt isolates sampled from wheat and other grasses distributed across the wheat-growing region of Brazil to estimate gene flow, assess the importance of sexual reproduction, and compare the genetic structures of Pygt populations infecting wheat and nearby grasses. Our results suggest a mixed reproductive system that includes sexual recombination as well as high levels of gene flow among regions, including evidence for higher gene flow from grass-infecting populations and into wheat-infecting populations than vice versa. The most common virulence groups were shared between the grass- and wheat-infecting Pygt populations, providing additional evidence for movement of Pygt between wheat fields and nearby grasses. Analyses of fruiting body formation found that proto-perithecia and perithecia developed on senescing stems of wheat and other grass hosts, suggesting that sexual reproduction occurs mainly during the saprotrophic phase of the disease cycle on dead residues. Phalaris canariensis (canarygrass) supported the fullest development of perithecia, suggesting it is a promising candidate for identifying the teleomorph in the field. Based on these findings, we formulated a more detailed disease cycle for wheat blast that includes an important role for grasses growing near wheat fields. Our findings strongly suggest that widely grown pasture grasses function as a major reservoir of wheat blast inoculum and provide a temporal and spatial bridge that connects wheat fields across Brazil.\n\nAuthor summaryAfter the first wheat blast epidemic occurred in 1985 in Parana, Brazil, the disease spread to Bolivia, Argentina, and Paraguay, and was introduced into Bangladesh in 2016 followed by India in 2017. Wheat blast is caused by Pyricularia graminis-tritici (Pygt), a highly diverse pathogen species related to the rice blast fungus P. oryzae, but with an independent origin and a broader host range. We conducted a large scale contemporary sampling of Pygt from symptomatic wheat and other grass species across Brazil and analyzed the genetic structure of Pygt populations. Pygt populations on both wheat and other grasses had high genotypic and virulence diversity, a genetic structure consistent with a mixed reproductive system that includes regular cycles of recombination. The pathogen formed sexual fruiting structures (perithecia) on senescing stems of wheat and other grasses. Historical migration analyses indicated that the majority of gene flow has been from Pygt populations on other grasses and into the Pygt population infecting wheat, consistent with the hypothesis that Pygt originated on other grasses before becoming a wheat pathogen. We found that the Pygt populations infecting wheat were indistinguishable from the Pygt populations infecting other grass species, including signal grass (Urochloa brizantha). Because U. brizantha is a widely grown grass pasture often found next to wheat fields, we propose that it functions as reservoir of Pygt inoculum that provides a temporal and spatial bridge that connects wheat fields in Brazil.

plant biology↗