Annual review of phytopathology最新文献

As obligate intracellular parasites, viruses depend entirely on host cells for propagation, with replication being the central process in establishing their infections. Upon entry into host cells, positive-strand RNA viruses induce rearrangement of the host's cellular membranes, leading to the formation of virus replication organelles (ROs). Advancements in imaging techniques have enabled the determination of three-dimensional structures for several plant viral ROs that are associated with specific organelle membranes and display either spherule- or tubule-shaped structures. Viral replication proteins, along with diversely recruited host factors such as lipids and membrane-shaping proteins, are used to remodel cellular membranes and build ROs. These ROs not only shield viral replication templates and intermediates from host defense mechanisms but also serve as efficient machinery for the synthesis of viral RNAs. Moreover, ROs are intricately connected to other stages of the viral life cycle, often triggering stress responses and redox shifts within the cellular microenvironment, positioning the ROs as central hubs for virus-plant interactions.

Trunk diseases are global wood diseases of grapevine that can significantly reduce the productive lifespan of vineyards. Infection may initiate at the nursery or in vineyards. Grapevine trunk diseases (GTDs) are caused by diverse Ascomycota and Basidiomycota fungal pathogens in at least nine families. They may be soilborne or airborne, depending on the type of pathogen involved, and can affect vineyards of all ages. GTDs constitute a complex group of diseases with multiple pathogens involved, diverse infection pathways, and a broad range of symptoms. Here, we discuss various aspects of GTDs, including their discovery and worldwide distribution, disease incidence in vineyards, pathogen taxonomy, and the most informative loci for identification as well as disease cycles and biology and plant-pathogen interaction. We also provide a review of the main control strategies employed to mitigate the impact of GTDs in nurseries and vineyards and discuss the main challenges for disease management and future needs.

Annual ryegrass toxicity (ARGT) has caused significant economic damage in Australia. This syndrome occurs when Rathayibacter toxicus is carried by a seed gall nematode into the developing seeds of forage grasses, where it produces a tunicamycin toxin. Grazing animals feeding on infected plants die when they consume sufficient toxin. Consequently, the Animal and Plant Health Inspection Service of the US Department of Agriculture listed R. toxicus as a plant pathogen select agent in the United States. The seed gall nematodes Anguina agrostis, Anguina funesta, Anguina paludicola, and Anguina tritici are regulated or quarantine pests in several countries. A. funesta and A. paludicola are of particular concern because they are the primary vectors of R. toxicus. Several new Rathayibacter species and nematode associations have been described, and we have gained a better understanding of toxin production in R. toxicus and other Rathayibacter species. This review focuses on R. toxicus and other Rathayibacter species; discusses their nematode vectors, distribution, diagnostics, and genomics; and provides suggestions for pathogen risk assessment, surveillance, and management of ARGT.

The Triticeae tribe comprises species representing some of the world's largest food and forage crops, including common wheat, durum, barley, rye, and oat. Crop yields are continuously threatened by various plant diseases and deploying disease resistance (R) genes is a key strategy for protection. More than 70 different Triticeae R gene loci have been cloned, with approximately 60% derived from wild relatives. These R genes belong to diverse protein families, such as receptor kinases (RKs), nucleotide-binding leucine-rich repeat (NLR) immune receptors, tandem kinase proteins, and kinase fusion proteins as well as noncanonical R genes related to membrane, transcription, and detoxification. RKs and NLRs often confer race-specific resistance by recognizing pathogen effectors, whereas noncanonical R genes can provide broad-spectrum resistance. This review provides an overview of the diverse R genes cloned from Triticeae and their evolutionary origins, modes of action, and application in resistance breeding.

To communicate across scientific disciplines, regulatory bodies, and the agricultural community, the naming of plant pathogens assigned to specific taxa is critical. Here, we provide an overview of the nomenclatural systems governing the naming of plant-pathogenic nematodes, fungi, oomycetes, prokaryotes, and viruses. Although we focus on the nature of the nomenclatural codes, we briefly discuss fundamental principles of taxonomy, including classification and identification. Key elements of the codes of nomenclature that ensure stability and clarity when naming species of pathogens are defined. When comparing the practice of nomenclature across different kingdoms, the classification and nomenclatural systems differ, and thus unique challenges are faced. We provide guidance from the codes and current practice for naming novel species. When there are nomenclatural conflicts, international committees play a critical role in their resolution. They also play a role in updating the codes to reflect new advancements in science. With this review, we aim to assist plant pathologists, journal editors, and those in related fields by providing an entrée to the legalistic requirements of the codes. Authors must consult and follow the rules of the appropriate code for any proposal of new or new combinations of names. To those interested in naming new species (or renaming the current ones), we recommend collaborations with experts in the field of taxonomy to ensure that rules for accurate and consistent naming practices and procedures are followed and to increase the likelihood that the proposed nomenclature is correct and acceptable.

This review focuses on the intricate interaction mechanisms between necrotrophic fungal pathogens and their host plants, emphasizing the pivotal role of effectors in orchestrating host cell death and immune responses. It undertakes a comparative analysis of effector-target interactions, contrasting those of broad-host-range necrotrophic fungal pathogens with host-specific necrotrophic fungal pathogens as well as necrotrophic fungal pathogens with biotrophic fungal pathogens. A detailed discussion is provided on how these effector mechanisms shape infection strategies. Additionally, the review introduces new disease control strategies and evaluates their advantages and limitations. Finally, in light of the effector interaction mechanisms, it advocates for the incorporation of artificial intelligence in future research and disease management efforts, aiming at expediting comprehension of effector-target interactions and developing novel strategies for disease control.

Plants have coevolved together with the microbes that surround them and this assemblage of host and microbes functions as a discrete ecological unit called a holobiont. This review outlines plant-driven assembly of disease-suppressive microbiomes. Plants are colonized by microbes from seed, soil, and air but selectively shape the microbiome with root exudates, creating microenvironment hot spots where microbes thrive. Using plant immunity for gatekeeping and surveillance, host-plant genetic properties govern microbiome assembly and can confer adaptive advantages to the holobiont. These advantages manifest in disease-suppressive soils, where buildup of specific microbes inhibits the causal agent of disease, that typically develop after an initial disease outbreak. Based on disease-suppressive soils such as take-all decline, we developed a conceptual model of how plants in response to pathogen attack cry for help and recruit plant-protective microbes that confer increased resistance. Thereby, plants create a soilborne legacy that protects subsequent generations and forms disease-suppressive soils.