Annual review of phytopathology最新文献

Harvested fruit and vegetables are perishable, subject to desiccation, show increased respiration during ripening, and are colonized by postharvest fungal pathogens. Induced resistance is a strategy to control diseases by eliciting biochemical processes in fruits and vegetables. This is accomplished by modulating the progress of ripening and senescence, which maintains the produce in a state of heightened resistance to decay-causing fungi. Utilization of induced resistance to protect produce has been improved by scientific tools that better characterize physiological changes in plants. Induced resistance slows the decline of innate immunity after harvest and increases the production of defensive responses that directly inhibit plant pathogens. This increase in defense response in fruits and vegetables contributes to higher amounts of phenols and antioxidant compounds, improving both the quality and appearance of the produce. This review summarizes mechanisms and treatments that induce resistance in harvested fruits and vegetables to suppress fungal colonization. Moreover, it highlights the importance of host maturity and stage of ripening as limiting conditions for the improved expression of induced-resistance processes.

Plant bacterial pathogens rely on host-derived signals to coordinate the deployment of virulence factors required for infection. In this review, I describe how diverse plant-pathogenic bacteria detect and respond to plant-derived metabolic signals for the purpose of virulence gene regulation. I highlight examples of how pathogens perceive host metabolites through membrane-localized receptors as well as intracellular response mechanisms. Furthermore, I describe how individual strains may coordinate their virulence using multiple distinct host metabolic signals, and how plant signals may positively or negatively regulate virulence responses. I also describe how plant defenses may interfere with the perception of host metabolites as a means to dampen pathogen virulence. The emerging picture is that recognition of host metabolic signals for the purpose of virulence gene regulation represents an important primary layer of interaction between pathogenic bacteria and host plants that shapes infection outcomes.

The plant immune system perceives pathogens to trigger defense responses. In turn, pathogens secrete effector molecules to subvert these defense responses. The initiation and maintenance of defense responses involve not only de novo synthesis of regulatory proteins and enzymes but also their regulated degradation. The latter is achieved through protein degradation pathways such as the ubiquitin-proteasome system (UPS). The UPS regulates all stages of immunity, from the perception of the pathogen to the execution of the response, and, therefore, constitutes an ideal candidate for microbial manipulation of the host. Pathogen effector molecules interfere with the plant UPS through several mechanisms. This includes hijacking general UPS functions or perturbing its ability to degrade specific targets. In this review, we describe how the UPS regulates different immunity-related processes and how pathogens subvert this to promote disease.

Since the 1950s, there have been major changes in the scope, value, and organization of the ornamental plant industry. With fewer individual producers and a strong trend toward consolidation and globalization, increasing quantities of diverse plant genera and species are being shipped internationally. Many more ornamentals are propagated vegetatively instead of by seed, further contributing to disease spread. These factors have led to global movement of pathogens to countries where they were not formerly known. The emergence of some previously undescribed pathogens has been facilitated by high-throughput sequencing, but biological studies are often lacking, so their roles in economic diseases are not yet known. Case studies of diseases in selected ornamentals discuss the factors involved in their spread, control measures to reduce their economic impact, and some potential effects on agronomic crops. Advances in diagnostic techniques are discussed, and parallels are drawn to the international movement of human diseases.

Plant disease control requires novel approaches to mitigate the spread of and losses caused by current, emerging, and re-emerging diseases and to adapt plant protection to global climate change and the restrictions on the use of conventional pesticides. Currently, disease management relies mainly on biopesticides, which are required for the sustainable use of plant-protection products. Functional peptides are candidate biopesticides because they originate from living organisms or are synthetic analogs and provide novel mechanisms of action against plant pathogens. Hundreds of compounds exist that cover an extensive range of activities against viruses, bacteria and phytoplasmas, fungi and oomycetes, and nematodes. Natural sources, chemical synthesis, and biotechnological platforms may provide peptides at large scale for the industry and growers. The main challenges for their use in plant disease protection are (a) the requirement of stability in the plant environment and counteracting resistance in pathogen populations, (b) the need to develop suitable formulations to increase their shelf life and methods of application, (c) the selection of compounds with acceptable toxicological profiles, and (d) the high cost of production for agricultural purposes. In the near future, it is expected that several functional peptides will be commercially available for plant disease control, but more effort is needed to validate their efficacy at the field level and fulfill the requirements of the regulatory framework.

Society is confronted by interconnected threats to ecological sustainability. Among these is the devastation of forests by destructive non-native pathogens and insects introduced through global trade, leading to the loss of critical ecosystem services and a global forest health crisis. We argue that the forest health crisis is a public-good social dilemma and propose a response framework that incorporates principles of collective action. This framework enables scientists to better engage policymakers and empowers the public to advocate for proactive biosecurity and forest health management. Collective action in forest health features broadly inclusive stakeholder engagement to build trust and set goals; accountability for destructive pest introductions; pooled support for weakest-link partners; and inclusion of intrinsic and nonmarket values of forest ecosystems in risk assessment. We provide short-term and longer-term measures that incorporate the above principles to shift the societal and ecological forest health paradigm to a more resilient state.

Plant and soil microbiomes are integral to the health and productivity of plants and ecosystems, yet researchers struggle to identify microbiome characteristics important for providing beneficial outcomes. Network analysis offers a shift in analytical framework beyond "who is present" to the organization or patterns of coexistence between microbes within the microbiome. Because microbial phenotypes are often significantly impacted by coexisting populations, patterns of coexistence within microbiomes are likely to be especially important in predicting functional outcomes. Here, we provide an overview of the how and why of network analysis in microbiome research, highlighting the ways in which network analyses have provided novel insights into microbiome organization and functional capacities, the diverse network roles of different microbial populations, and the eco-evolutionary dynamics of plant and soil microbiomes.

Tomato brown rugose fruit virus (ToBRFV) is an emerging tobamovirus. It was first reported in 2015 in Jordan in greenhouse tomatoes and now threatens tomato and pepper crops around the world. ToBRFV is a stable and highly infectious virus that is easily transmitted by mechanical means and via seeds, which enables it to spread locally and over long distances. The ability of ToBRFV to infect tomato plants harboring the commonly deployed Tm resistance genes, as well as pepper plants harboring the L resistance alleles under certain conditions, limits the ability to prevent damage from the virus. The fruit production and quality of ToBRFV-infected tomato and pepper plants can be drastically affected, thus significantly impacting their market value. Herein, we review the current information and discuss the latest areas of research on this virus, which include its discovery and distribution, epidemiology, detection, and prevention and control measures, that could help mitigate the ToBRFV disease pandemic.

Understanding the coevolutionary history of plants, pathogens, and disease resistance is vital for plant pathology. Here, I review Francis O. Holmes's work with tobacco mosaic virus (TMV) framed by the foundational work of Nikolai Vavilov on the geographic centers of origin of plants and crop wild relatives (CWRs) and T. Harper Goodspeed's taxonomy of the genus Nicotiana. Holmes developed a hypothesis that the origin of host resistance to viruses was due to coevolution of both at a geographic center. In the 1950s, Holmes proved that genetic resistance to TMV, especially dominant R-genes, was centered in South America for Nicotiana and other solanaceous plants, including Capsicum, potato, and tomato. One seeming exception was eggplant (Solanum melongena). Not until the acceptance of plate tectonics in the 1960s and recent advances in evolutionary taxonomy did it become evident that northeast Africa was the home of eggplant CWRs, far from Holmes's geographic center for TMV-R-gene coevolution. Unbeknownst to most plant pathologists, Holmes's ideas predated those of H.H. Flor, including experimental proof of the gene-for-gene interaction, identification of R-genes, and deployment of dominant host genes to protect crop plants from virus-associated yield losses.

Membrane trafficking pathways play a prominent role in plant immunity. The endomembrane transport system coordinates membrane-bound cellular organelles to ensure that immunological components are utilized effectively during pathogen resistance. Adapted pathogens and pests have evolved to interfere with aspects of membrane transport systems to subvert plant immunity. To do this, they secrete virulence factors known as effectors, many of which converge on host membrane trafficking routes. The emerging paradigm is that effectors redundantly target every step of membrane trafficking from vesicle budding to trafficking and membrane fusion. In this review, we focus on the mechanisms adopted by plant pathogens to reprogram host plant vesicle trafficking, providing examples of effector-targeted transport pathways and highlighting key questions for the field to answer moving forward.