Red rot disease reduces sugarcane yield and impacts the sugar quality, posing an important threat to the sugarcane industry in Florida. Although Colletotrichum falcatum, the causal agent of red rot in Florida, was first reported in 1984 based on morphology, molecular and pathological data have remained limited, highlighting the critical need for comprehensive characterization. Thirteen isolates were obtained from three local sugarcane varieties in Belle Glade, Florida. Phylogenetic analyses of five genetic markers (ITS, ACT, TUB2, GAPDH, and CHS-1) confirmed all the strains as C. falcatum. In addition, the study documented the disease progression at the cellular level and assessed the pathogenicity of representative strains using the leaf sheath and whole-seedling inoculation methods. The varieties CP96-1252 and CP89-2143 showed greater host resistance. These findings represent the first report of C. falcatum causing red rot in southern Florida, offer valuable insights for/into red rot management, and provide a basis for future breeding programs to enhance sugarcane resistance to red rot disease.

Tan Spot disease is caused by the necrotrophic pathogen Pyrenophora tritici‐repentis (Ptr) and poses a significant threat to global wheat production. Therefore, novel sources of resistance need to be identified, coupled with a fuller mechanistic understanding of host responses to Ptr. Herein, we characterise the interaction between a ToxA‐positive Ptr strain and parental wheat lines from a multiparent advanced generation intercross (MAGIC) population. Genotypes displaying moderate resistance (‘Robigus’) or susceptibility (‘Hereward’) to Ptr challenge were identified and characterised through histological, metabolomic, and transcriptomic approaches. Histological investigations indicated the prominence of papilla‐based defences in Robigus. Transcriptomic analyses could link this to the expression of barrier‐related genes i.e. actin polymerisation, callose deposition, vesicle trafficking, and cellulose synthesis. Inhibiting actin polymerisation with cytochalasin E increased lesion numbers but did not augment lesion growth, suggesting the deployment of other defence mechanisms. These may be influenced by auxin, as its exogenous application exacerbated symptom development. Transcriptomic and metabolomic analyses in Hereward following challenge with Ptr suggested shifts in primary metabolism, affecting glycolysis, the TCA cycle, and the γ‐aminobutyric acid (GABA) shunt. Activation of salicylic acid (SA)‐associated genes, including NPR1 and WRKY33, was specific to Hereward, and exogenous SA increased susceptibility to Ptr in both genotypes. This study suggests barrier defences could be effective against Ptr as well as a lack of susceptibility factors like SA or the appropriate processing of IAA. These findings offer potential avenues for enhancing wheat resistance to Ptr.

Introduction: Tan Spot (TS) disease of wheat is caused by Pyrenophora tritici-repentis (Ptr), where most of the yield loss is linked to diseased flag leaves. As there are no fully resistant cultivars available, elucidating the responses of wheat to Ptr could inform the derivation of new resistant genotypes. Objectives: The study aimed to characterise the flag-leaf metabolomes of two spring wheat cultivars (Triticum aestivum L. cv. PF 080719 [PF] and cv. Fundacep Horizonte [FH]) following challenge with Ptr to gain insights into TS disease development. Methods: PF and FH plants were inoculated with a Ptr strain that produces the necrotrophic toxin ToxA. The metabolic changes in flag leaves following challenge (24, 48, 72, and 96 h post-inoculation [hpi]) with Ptr were investigated using untargeted flow infusion ionisation-high resolution mass spectroscopy (FIE-HRMS). Results: Both cultivars were susceptible to Ptr at the flag-leaf stage. Comparisons of Ptr- and mock-inoculated plants indicated that a major metabolic shift occurred at 24 hpi in FH, and at 48 hpi in PF. Although most altered metabolites were genotype specific, they were linked to common pathways; phenylpropanoid and flavonoid metabolism. Alterations in sugar metabolism as well as in glycolysis and glucogenesis pathways were also observed. Pathway enrichment analysis suggested that Ptr-triggered alterations in chloroplast and photosynthetic machinery in both cultivars, especially in FH at 96 hpi. In a wheat-Ptr interactome in integrative network analysis, “flavone and flavonol biosynthesis” and “starch and sucrose metabolism” were targeted as the key metabolic processes underlying PF–FH–Ptr interactions. Conclusion: These observations suggest the potential importance of flavone and flavonol biosynthesis as well as bioenergetic shifts in susceptibility to Ptr. This work highlights the value of metabolomic approaches to provide novel insights into wheat pathosystems.

Tar spot, a fungal foliar disease, affects most maize types commonly grown in Florida, such as sweet corn, field corn, and criollo corn. This disease is characterized by brown-to-black, raised structures called stromata, which are embedded in leaf tissue. As a polycyclic disease, tar spot lesions can increase in number as the disease progresses throughout the growing season, leading to reduction of photosynthetic area on the leaves. Tar spot has recently emerged as a significant threat in Florida and in the United States, with reports of up to 100% incidence in maize fields in south Florida. Tar spot occurrence and development in Florida is influenced by several factors, such as environmental conditions, maize types, crop maintenance, and corn growth stages. The purpose of this publication is to promote awareness among Florida growers regarding this newly identified disease and its management practices.

Fusarium wilt, caused by Fusarium oxysporum f. sp. apii (Foa), is a vascular disease affecting celery. This soilborne pathogen is classified into four distinct pathogenic races: 1, 2, 3, and 4. Notably, race 4 emerges as the most virulent, representing the latest evolutionary development of this pathogen, which was first reported in 2013 in California. In 2022, celery plants in South Florida exhibited typical Fusarium wilt symptoms, with the disease reaching a 100% incidence and causing yield losses ranging from 20 to 100%. Given the significance of celery as a vegetable crop and the severity of this outbreak, the primary objective of this study was to identify and characterize the causal agent of Fusarium wilt in South Florida. The second goal aimed to test the pathogenicity and virulence of the Fusarium isolates from Florida on celery and parsley plants. Using race-specific primers and dual-loci phylogenetic analyses, the isolates surveyed in this study were identified as Foa race 4. Pathogenicity assays in the greenhouse showed that the Foa race 4 isolate from celery induced disease not only on the two celery cultivars (Duda 30 and Duda 71) but also on two commonly cultivated parsley varieties (curly and Italian). Our study also revealed that the Foa race 4 significantly (P < 0.05) affected plant health attributes in all cultivars, including plant height, total plant weight, and root weight. Interestingly, the pathogen exhibited higher (P < 0.0001) virulence on parsley than celery based on vascular discoloration. These findings strongly indicate the urgency of comprehending and managing Fusarium wilt on celery and related crops. Furthermore, the ability of Foa race 4 to affect different plant species highlights a potential threat to agricultural production, emphasizing the need for proactive measures to mitigate the impact of this virulent pathogen.

Pyrenophora tritici-repentis (Ptr), the causal agent of tan spot, is a necrotrophic fungus that represents a significant threat to wheat production worldwide. The development of resistant cultivars is limited by an incomplete understanding of wheat defence responses against Ptr. Here, weighted gene co-expression network analysis (WGCNA) was applied to RNA-seq data from resistant (Robigus) and susceptible (Hereward) wheat lines before and after Ptr infection to identify coordinated host responses. Eight co-expression modules were identified, three of which were linked to either resistance, susceptibility, or Ptr infection. The resistance-associated module was enriched with chloroplast ribosomal machinery genes (e.g., 50S ribosome-binding GTPase, L28, L6), and transcriptional regulators. This suggested that maintaining chloroplast function, coupled with large-scale transcriptional reprogramming, was important for resistance. The susceptibility-associated module indicated the high expression of post-transcriptional modifiers, including SGS3, RBX1, and SENPs. The Ptr-responsive module showed common responses in both genotypes and included several defence-related genes (nucleotide-binding domain leucine-rich repeat R-genes [NLRs], chitinases, beta-1,3-glucanases) and metabolic pathways, such as phenylpropanoid biosynthesis and nitrogen metabolism (phenylpropanoid ammonia lyase [PAL], cytochrome P450s, glutamine synthase, and ammonium transporters). These results define distinct and shared molecular networks that are linked to resistance and susceptibility, providing valuable candidate genes for functional validation that could ultimately be exploited to enhance wheat resilience against necrotrophic fungal pathogens.