RESUMO
Soybean rust (SBR), caused by the obligate biotrophic fungus Phakopsora pachyrhizi, is a devastating foliar disease threatening soybean production. To date, no commercial cultivars conferring durable resistance to SBR are available. The development of long-lasting SBR resistance has been hindered by the lack of understanding of this complex pathosystem, encompassing challenges posed by intricate genetic structures in both the host and pathogen, leading to a gap in the knowledge of gene-for-gene interactions between soybean and P. pachyrhizi. In this review, we focus on recent advancements and emerging technologies that can be used to improve our understanding of the P. pachyrhizi-soybean molecular interactions. We further explore approaches used to combat SBR, including conventional breeding, transgenic approaches and RNA interference, and how advances in our understanding of plant immune networks, the availability of new molecular tools, and the recent sequencing of the P. pachyrhizi genome could be used to aid in the development of better genetic resistance against SBR. Lastly, we discuss the research gaps of this pathosystem and how new technologies can be used to shed light on these questions and to develop durable next-generation SBR-resistant soybean plants.
Assuntos
Basidiomycota , Phakopsora pachyrhizi , Phakopsora pachyrhizi/genética , Glycine max/genética , Melhoramento Vegetal , Doenças das Plantas/genética , Doenças das Plantas/microbiologiaRESUMO
Asian soybean rust, caused by the fungus Phakopsora pachyrhizi, is one of the most important diseases affecting soybean production in tropical areas. During infection, P. pachyrhizi secretes proteins from haustoria that are transferred into plant cells to promote virulence. To date, only one candidate P. pachyrhizi effector protein has been characterized in detail to understand the mechanism by which it suppresses plant defenses to enhance infection. Here, we aimed to extend understanding of the pathogenic mechanisms of P. pachyrhizi based on the discovery of host proteins that interact with the effector candidate Phapa-7431740. We demonstrated that Phapa-7431740 suppresses pathogen-associated molecular pattern-triggered immunity (PTI) and that it interacts with a soybean glucan endo-1,3-ß-glucosidase (GmßGLU), a pathogenesis-related (PR) protein belonging to the PR-2 family. Structural and phylogenetic characterization of the PR-2 protein family predicted in the soybean genome and comparison to PR-2 family members in Arabidopsis thaliana and cotton, demonstrated that GmßGLU is a type IV ß-1,3-glucanase. Transcriptional profiling during an infection time course showed that the GmßGLU mRNA is highly induced during the initial hours after infection, coinciding with peak of expression of Phapa-7431740. The effector was able to interfere with the activity of GmßGLU in vitro, with a dose-dependent inhibition. Our results suggest that Phapa-7431740 may suppress PTI by interfering with glucan endo-1,3-ß-glucosidase activity. [Formula: see text] The author(s) have dedicated the work to the public domain under the Creative Commons CC0 "No Rights Reserved" license by waiving all of his or her rights to the work worldwide under copyright law, including all related and neighboring rights, to the extent allowed by law, 2022.