Legumes have played an important part in cropping systems since the dawn of agriculture, both as human food and as animal feed. The legume family is arguably one of the most abundantly domesticated crop plant families. Their ability to symbiotically fix nitrogen and improve soil fertility has been rewarded since antiquity and makes them a key protein source. The pea was the original model organism used in Mendel’s discovery of the laws of inheritance, making it the foundation of modern plant genetics. This Special Issue provides up-to-date information on legume biology, genetic advances, and the legacy of Mendel.

White mold caused by Sclerotinia sclerotiorum is an important constraint to field pea (Pisum sativum L.) production worldwide. To transfer white mold resistance into an adapted background, and study the genetics of the disease, two recombinant inbred line (RIL) populations (PRIL17 and PRIL19) were developed by crossing two partially resistant plant introductions with two susceptible pea cultivars. PRIL17 (Lifter × PI240515), and PRIL19 (PI169603 × Medora) were evaluated for resistance to white mold by measuring lesion expansion inhibition (LEI) and nodal transmission inhibition (NTI) at 3, 7, and 14 days post inoculation (dpi) under controlled environmental conditions. Lesion expansion inhibition percentage (LEIP), survival rate (SR), and area under disease progress curves (AUDPC) were also calculated accordingly. Because of a positive correlation between LEI and NTI with height, short and long internode individuals of each population were analyzed separately to avoid any confounding effect of height to pathogen response. A total of 22 short genotypes demonstrated partial resistance based on at least two Porter's resistance criteria. Only two pea genotypes with partial resistance to white mold (PRIL19-18 and PRIL19-124) had both semi-leafless (afila) and short internode traits. Both the RIL populations were genotyped using genotyping by sequencing (GBS). For PRIL17 and PRIL19, genetic maps were constructed from a total of 1,967 and 1,196 single nucleotide polymorphism (SNP) and spanned over 1,494 cM and 1,415 cM representing seven and nine linkage groups, respectively. A consensus map constructed using data from both populations, had 1,486 unique SNPs over 2,461 cM belonging to seven linkage groups. Inclusive composite interval mapping (ICIM) identified thirteen quantitative trait loci (QTL) associated with white mold resistance traits in both populations. Three of them were co-located with height genes (a morphological trait that reduces infection risk and acts as disease avoidance) and the other ten QTL were associated with two forms of physiological resistance (seven for LEI and three for NTI) with LOD and r² ranging from 3.0 to 28.5 and 5.1 to 64.3, respectively. The development of resistance lines, genetic dissection and identification of markers associated will help accelerate breeding efforts for white mold resistance using molecular breeding approaches.

Root rot caused by Fusarium spp. is a significant issue in the chickpea-growing regions of Montana. The specific Fusarium species responsible for the disease and their prevalence remain uncertain. A survey was conducted in 2020 and 2021 to identify Montana’s Fusarium species associated with chickpea. Four hundred and twenty-six Fusarium isolates were recovered from symptomatic chickpea roots across ten counties in the state. Isolates were identified by comparing translation elongation factor 1-α (TEF1-α) sequences in the FUSARIUM-ID database. Among the recovered isolates, Fusarium oxysporum was the most prevalent species (33%), followed by F. acuminatum (21%), F. avenaceum (15%), F. redolens (14%), F. culmorum (6%), F. sporotrichioides (6%), Neocosmospora solani (6%), F. equiseti (2%), F. torulosum (0.9%), F. gamsii (0.8%), F. proliferatum (0.2%), F. pseudograminearum (0.2%), and F. brachygibbosum (0.1%). The aggressiveness of a subset of 51 isolates representing various Fusarium spp. was tested on chickpea cv. ‘CDC Frontier’. A non-parametric variance analysis conducted on disease severity ranks indicated that F. avenaceum isolates were highly aggressive. This study reports for the first time that F. gamsii, F. proliferatum and F. brachygibbosum are causal agents of root rot in chickpea in the United States. This knowledge is invaluable for making informed decisions regarding crop rotation, disease management, and developing resistant chickpea varieties against economically significant Fusarium pathogens.

Ascochyta blight (AB) is a destructive disease of the field pea (Pisum sativum L.) caused by necrotrophic fungal pathogens known as the AB-disease complex. To identify resistant individuals to assist AB resistance breeding, low-cost, high throughput, and reliable protocols for AB screening are needed. We tested and optimized three protocols to determine the optimum type of pathogen inoculum, the optimal development stage for host inoculation, and the timing of inoculation for detached-leaf assays. We found that different plant development stages do not affect AB infection type on peas, but the timing of inoculation affects the infection type of detached leaves due to wound-induced host defense response. After screening nine pea cultivars, we discovered that cultivar Fallon was immune to A. pisi but not to A. pinodes or the mixture of the two species. Our findings suggest that AB screening can be done with any of the three protocols. A whole-plant inoculation assay is necessary for identifying resistance to stem/node infection. Pathogen inoculation must be completed within 1.5 h post-detachment to avoid false positives of resistance for detach-leaf assays. It is essential to use a purified single-species inoculum for resistant resource screenings to identify the host resistance to each single species.

The disease white mold caused by the fungus Sclerotinia sclerotiorum is a significant threat to pea production and improved resistance to this disease is needed. Nodal resistance in plants is a phenomenon where a fungal infection is prevented from passing through a node and the infection is limited to an internode region. Nodal resistance has been observed in some pathosystems such as the pea ( Pisum sativum L.)- S. sclerotiorum pathosystem. Other than nodal resistance, different pea lines display different levels of stem lesion size restriction, referred to as lesion resistance. It is unclear whether the genetics of lesion resistance and nodal resistance are identical or different. This study applied genome-wide association studies (GWAS) and RNA-Seq to understand the genetic makeup of these two types of resistance. The time series RNA-Seq experiment consisted of two pea lines (the susceptible ‘Lifter’ and the partially resistant PI 240515), two treatments (mock samples and S. sclerotiorum inoculated samples), and three time points (12, 24, and 48 hours post-inoculation). Integrated results from GWAS and RNA-Seq analyses identified different redox-related transcripts for lesion and nodal resistances. A transcript encoding a glutathione S-transferase was the only shared resistance source for both phenotypes. There were more leucine rich-repeat containing transcripts found for lesion resistance, while different candidate resistance transcripts such as a VQ motif-containing protein and a myo-inositol oxygenase were found for nodal resistance. This study demonstrated the robustness of combining GWAS and RNA-Seq for identifying white mold resistance in pea, and results suggest different genetics underlying lesion and nodal resistance.