The Soybean Rpp3 Gene Encodes a TIR-NBS-LRR Protein that Confers Resistance to Phakopsora pachyrhizi.

Soybean rust is an economically significant disease caused by the fungus Phakopsora pachyrhizi that negatively impacts soybean (Glycine max [L.] Merr.) production throughout the world. Susceptible plants infected by P. pachyrhizi develop tan-colored lesions on the leaf surface that give rise to funnel-shaped uredinia as the disease progresses. While most soybean germplasm is susceptible, seven genetic loci (Rpp1 to Rpp7) that provide race-specific resistance to P. pachyrhizi (Rpp) have been identified. Rpp3 was first discovered and characterized in the soybean accession PI 462312 (Ankur), and it was also determined to be one of two Rpp genes present in PI 506764 (Hyuuga). Genetic crosses with PI 506764 were later used to fine-map the Rpp3 locus to a 371-kb region on chromosome 6. The corresponding region in the susceptible Williams 82 (Wm82) reference genome contains several homologous nucleotide binding site-leucine rich repeat (NBS-LRR) genes. To identify Rpp3, we designed oligonucleotide primers to amplify Rpp3 candidate (Rpp3C) NBS-LRR genes at this locus from PI 462312, PI 506764, and Wm82 using polymerase chain reaction (PCR). Five Rpp3C genes were identified in both Rpp3-resistant soybean lines, and co-silencing these genes compromised resistance to P. pachyrhizi. Gene expression analysis and sequence comparisons of the Rpp3C genes in PI 462312 and PI 506764 suggest that a single candidate gene, Rpp3C3, is responsible for Rpp3-mediated resistance. [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, 2024.

Uncovering the environmental conditions required for Phyllachora maydis infection and tar spot development on corn in the United States for use as predictive models for future epidemics.

Phyllachora maydis is a fungal pathogen causing tar spot of corn (Zea mays L.), a new and emerging, yield-limiting disease in the United States. Since being first reported in Illinois and Indiana in 2015, P. maydis can now be found across much of the corn growing regions of the United States. Knowledge of the epidemiology of P. maydis is limited but could be useful in developing tar spot prediction tools. The research presented here aims to elucidate the environmental conditions necessary for the development of tar spot in the field and the creation of predictive models to anticipate future tar spot epidemics. Extended periods (30-day windowpanes) of moderate mean ambient temperature (18-23 °C) were most significant for explaining the development of tar spot. Shorter periods (14- to 21-day windowpanes) of moisture (relative humidity, dew point, number of hours with predicted leaf wetness) were negatively correlated with tar spot development. These weather variables were used to develop multiple logistic regression models, an ensembled model, and two machine learning models for the prediction of tar spot development. This work has improved the understanding of P. maydis epidemiology and provided the foundation for the development of a predictive tool for anticipating future tar spot epidemics.

Molecular and physiological characterization of six-way resistance in an Amaranthus tuberculatus var. rudis biotype from Missouri.

BACKGROUND: Previous research reported the first case of six-way herbicide resistance in a common waterhemp (Amaranthus tuberculatus var. rudis) biotype from Missouri, USA designated MO-Ren. This study investigated the mechanisms of multiple-resistance in the MO-Ren biotype to herbicides from six site-of-action (SOA) groups, i.e. synthetic auxins, 5-enolypyruvyl-shikimate-3-phosphate synthase (EPSPS)-, protoporphyrinogen oxidase (PPO)-, acetolactate synthase (ALS)-, photosystem II (PSII)-, and 4-hydroxyphenyl-pyruvate-dioxygenase (HPPD)-inhibitors. RESULTS: Genomic DNA sequencing confirmed the presence of known mutations associated with ALS- or PPO-inhibiting herbicide resistance: the Trp-574-Leu amino acid substitution in the ALS enzyme and the codon deletion corresponding to the ΔG210 in the PPX2 enzyme. No target-site point mutations associated with resistance to PSII- and EPSPS-inhibitors were detected. Quantitative polymerase chain reaction (qPCR) indicated that MO-Ren plants contained five-fold more copies of the EPSPS gene than susceptible plants. Malathion in combination with 2,4-D (2,4-dichlorophenoxyacetic acid), mesotrione, and chlorimuron POST enhanced the activity of these herbicides indicating that metabolism due to cytochrome P450 monooxygenase activity was involved in herbicide resistance. 4-Chloro-7-nitrobenzofurazan (NBD-Cl), a glutathione-S-transferase (GST)-inhibitor, in combination with atrazine did not reduce the biomass accumulation. Reduced absorption or translocation of 2,4-D did not contribute to resistance. However, the resistant biotype metabolized 2,4-D, seven- to nine-fold faster than the susceptible. CONCLUSION: Target-site point mutations, gene amplification, and elevated rates of metabolism contribute to six-way resistance in the MO-Ren biotype, suggesting both target site and non-target site mechanisms contribute to multiple herbicide resistance in this Amaranthus tuberculatus biotype. © 2018 Society of Chemical Industry.