We report a fungal pan-genome study involving Parastagonospora spp., including 21 isolates of the wheat (Triticum aestivum) pathogen Parastagonospora nodorum, 10 of the grass-infecting Parastagonospora avenae, and 2 of a closely related undefined sister species. We observed substantial variation in the distribution of polymorphisms across the pan-genome, including repeat-induced point mutations, diversifying selection and gene gains and losses. We also discovered chromosome-scale inter and intraspecific presence/absence variation of some sequences, suggesting the occurrence of one or more accessory chromosomes or regions that may play a role in host-pathogen interactions. The presence of known pathogenicity effector loci SnToxA, SnTox1, and SnTox3 varied substantially among isolates. Three P. nodorum isolates lacked functional versions for all three loci, whereas three P. avenae isolates carried one or both of the SnTox1 and SnTox3 genes, indicating previously unrecognized potential for discovering additional effectors in the P. nodorum-wheat pathosystem. We utilized the pan-genomic comparative analysis to improve the prediction of pathogenicity effector candidates, recovering the three confirmed effectors among our top-ranked candidates. We propose applying this pan-genomic approach to identify the effector repertoire involved in other host-microbe interactions involving necrotrophic pathogens in the Pezizomycotina.
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http://dx.doi.org/10.1093/gbe/evy192 | DOI Listing |
Sci Transl Med
January 2025
Division of Pediatric Hematology/Oncology, Boston Children's Hospital, Boston, MA 02115, USA.
Tissue-specific T cell immune responses play a critical role in maintaining organ health but can also drive immune pathology during both autoimmunity and alloimmunity. The mechanisms controlling intratissue T cell programming remain unclear. Here, we leveraged a nonhuman primate model of acute graft-versus-host disease (aGVHD) after allogeneic hematopoietic stem cell transplantation to probe the biological underpinnings of tissue-specific alloimmune disease using a comprehensive systems immunology approach including multiparameter flow cytometry, population-based transcriptional profiling, and multiplexed single-cell RNA sequencing and TCR sequencing.
View Article and Find Full Text PDFSci Adv
January 2025
State Key Laboratory of Ecological Pest Control for Fujian and Taiwan Crops, Institute of Plant Virology, Fujian Agriculture and Forestry University, Fuzhou, Fujian, China.
Insect melanization triggered by the conversion of prophenoloxidase to active phenoloxidase via serine proteases (SPs) is an important immediate immune response. However, how phytoplasmas evade this immune response to promote their propagation in insect vectors remains unknown. Here, we demonstrate that infection of leafhopper vectors with rice orange leaf phytoplasma (ROLP) activates the mild melanization response in hemolymph.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
February 2025
Department of Molecular Microbiology, Washington University in St. Louis, School of Medicine, St. Louis, MO 63130.
bradyzoites reside in tissue cysts that undergo cycles of expansion, rupture, and release to foster chronic infection. The glycosylated cyst wall acts as a protective barrier, although the processes responsible for formation, remodeling, and turnover are not understood. Herein, we identify a noncanonical chitinase-like enzyme TgCLP1 that localizes to micronemes and is targeted to the cyst wall after secretion.
View Article and Find Full Text PDFmBio
January 2025
University of Angers, Brest University, IRF, SFR ICAT, Angers, France.
The emerging fungal pathogen is known for its strong skin tropism and resilience against antifungal and disinfection treatment, posing a significant challenge for healthcare units. Although efforts to identify the effectors of its unique pathogenic behavior have been insightful, the role of the high-osmolarity glycerol (HOG) pathway in this context remains unexplored. The study by Shivarathri and co-workers (R.
View Article and Find Full Text PDFmBio
January 2025
Department of Microbiology and Immunology, University of Rochester Medical Center, Rochester, New York, USA.
Unlabelled: Pathogenic strains cause cholera using different mechanisms. O1 and O139 serogroup strains use the toxin-co-regulated pilus (TCP) and cholera toxin (CT) for intestinal colonization and to promote secretory diarrhea, while non-O1/non-O139 serogroup strains are typically non-toxigenic and use alternate virulence factors to cause a clinically similar disease. An O39 serogroup, TCP/CT-negative strain, named AM-19226, uses a type III secretion system (T3SS) to translocate more than 10 effector proteins into the host cell cytosol.
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