Project description:The soft rot pathogen Janthinobacterium agaricidamnosum causes devastating damage to button mushrooms (Agaricus bisporus), one of the most cultivated and commercially relevant mushrooms. We previously discovered that this pathogen releases the membrane-disrupting lipopeptide jagaricin. This bacterial toxin, however, could not solely explain the rapid decay of mushroom fruiting bodies, indicating that J. agaricidamnosum implements a more sophisticated infection strategy. In this study, we show that secretion systems play a crucial role in soft rot disease. By mining the genome of J. agaricidamnosum, we identified gene clusters encoding a type I (T1SS), a type II (T2SS), a type III (T3SS), and two type VI secretion systems (T6SS). Through a combination of knockout studies and bioassays, we found that the T2SS and T3SS of J. agaricidamnosum are required for soft rot disease. Furthermore, comparative secretome analysis and activity-guided fractionation identified a number of secreted lytic enzymes responsible for mushroom damage. Our findings regarding the contribution of secretion systems to the disease process expand the current knowledge of bacterial soft rot pathogens and represent a significant stride towards identifying targets for their disarmament with secretion system inhibitors.
2023-07-02 | PXD040852 | Pride
Project description:Soft rot pathogen of the konjac
Project description:Soft rot or Rhizopus rot, caused by the fungal pathogen Rhizopus stolonifer, is an aggressive postharvest disease that affects many fruit and vegetables. We proposed that R. stolonifer displays a necrotrophic behavior when infecting fruit, actively killing the host tissues to complete its life cycle. We tested this hypothesis by identifying R. stolonifer infection strategies when interacting with four fruit hosts (tomato, grape, strawberry, and plum). First, we generated a complete and highly contiguous genome assembly for R. stolonifer using PacBio sequencing, of 45.02 Mb in size, an N50 of 2.87Mb, and 12,644 predicted loci with protein-coding genes. We then performed a transcriptomic analysis to identify genes preferentially used by R. stolonifer when growing in fruit versus culture media, and then classified these host-related genes into clusters according to their expression patterns across four time points. Based on the expression data, we determined that R. stolonifer deploys infection mechanisms characteristic of necrotrophs, including a suite of oxidases, proteases, and cell wall degrading enzymes, when it is actively breaking down tissues of all four fruit hosts. Better understanding R. stolonifer – fruit host interactions can support better diagnostic tools and efficient management strategies in postharvest.