Genome-Wide Association Study (GWAS) of White Mold Resistance in Snap Bean.

White mold can result in snap bean yield losses of 90 to 100% when field conditions favor the pathogen. A genome-wide association study (GWAS) was conducted to detect loci significantly associated with white mold resistance in a panel of snap bean ( L.) cultivars.

Associated SNPs, Heritabilities, Trait Correlations, and Genomic Breeding Values for Resistance in Snap Beans ( L.) to Root Rot Caused by (Mart.) f. sp. (Burkholder).

Root rot is a major constraint to snap bean () production in the United States and around the world. Genetic resistance is needed to effectively control root rot disease because cultural control methods are ineffective, and the pathogen will be present at the end of one season of production on previously clean land. A diversity panel of 149 snap bean pure lines was evaluated for resistance to root rot in Oregon.

Improving the Health Benefits of Snap Bean: Genome-Wide Association Studies of Total Phenolic Content.

Snap beans are a significant source of micronutrients in the human diet. Among the micronutrients present in snap beans are phenolic compounds with known beneficial effects on human health, potentially via their metabolism by the gut-associated microbiome. The genetic pathways leading to the production of phenolics in snap bean pods remain uncertain.

Identification and spontaneous immune targeting of an endogenous retrovirus K envelope protein in the Indian rhesus macaque model of human disease.

Background: Endogenous retroviruses (ERVs) are remnants of ancient retroviral infections that have invaded the germ line of both humans and non-human primates. Most ERVs are functionally crippled by deletions, mutations, and hypermethylation, leading to the view that they are inert genomic fossils. However, some ERVs can produce mRNA transcripts, functional viral proteins, and even non-infectious virus particles during certain developmental and pathological processes.

Simian immunodeficiency virus-specific CD4+ T cells from successful vaccinees target the SIV Gag capsid.

We recently demonstrated that vaccinated rhesus macaques controlled viral replication of a heterologous SIV challenge. Here, we analyzed anamnestic SIV-specific CD4+ T-cell responses expanding immediately after challenge and show that successful vaccinees consistently targeted a short region of the Gag-p27 Capsid (amino acids 249-291). We have also defined the major histocompatibility complex class II (MHC-II) restricting alleles for several of these responses and show that DQ-restricted CD4+ T-cells depend on unique combinations of both the DQA and DQB alleles.

Simian immunodeficiency virus-specific CD8+ T cells recognize Vpr- and Rev-derived epitopes early after infection.

The kinetics of CD8(+) T cell epitope presentation contribute to the antiviral efficacy of these cells yet remain poorly defined. Here, we demonstrate presentation of virion-derived Vpr peptide epitopes early after viral penetration and prior to presentation of Vif-derived epitopes, which required de novo Vif synthesis. Two Rev epitopes exhibited differential presentation kinetics, with one Rev epitope presented within 1 h of infection.

Gag- and Nef-specific CD4+ T cells recognize and inhibit SIV replication in infected macrophages early after infection.

The precise immunological role played by CD4(+) T cells in retroviral infections is poorly defined. Here, we describe a new function of these cells, the elimination of retrovirus-infected macrophages. After experimental CD8(+) cell depletion, elite controlling macaques with set-point viral loads < or = 500 viral RNA copies/mL mounted robust Gag- and Nef-specific CD4(+) T cell responses during reestablishment of control with > or = 54% of all virus-specific CD4(+) T cells targeting these 2 proteins.

Mauritian cynomolgus macaques share two exceptionally common major histocompatibility complex class I alleles that restrict simian immunodeficiency virus-specific CD8+ T cells.

Vaccines that elicit CD8(+) T-cell responses are routinely tested for immunogenicity in nonhuman primates before advancement to clinical trials. Unfortunately, the magnitude and specificity of vaccine-elicited T-cell responses are variable in currently utilized nonhuman primate populations, owing to heterogeneity in major histocompatibility (MHC) class I genetics. We recently showed that Mauritian cynomolgus macaques (MCM) have unusually simple MHC genetics, with three common haplotypes encoding a shared pair of MHC class IA alleles, Mafa-A*25 and Mafa-A*29.

Differential antigen presentation kinetics of CD8+ T-cell epitopes derived from the same viral protein.

The kinetics of peptide presentation by major histocompatibility complex class I (MHC-I) molecules may contribute to the efficacy of CD8+ T cells. Whether all CD8+ T-cell epitopes from a protein are presented by the same MHC-I molecule with similar kinetics is unknown. Here we show that CD8+ T-cell epitopes derived from SIVmac239 Gag are presented with markedly different kinetics.

Recombination within mouse t haplotypes has replaced significant segments of t-specific DNA.

Previous studies on the fourth inversion of the t complex, In17(4), suggest that loci near the center of this inversion have been subjected to segmental recombination during the past 1-2 million years. We have used a combination of PCR-based restriction site (PBR) analysis and DNA sequencing to perform a high-resolution analysis of a 2-million base pair (Mbp) segment in the middle of In17(4). We examined 21 restriction sites that are polymorphic between t haplotypes and their wild-type homologs, over nine distinct loci.

CD8+ T cells from SIV elite controller macaques recognize Mamu-B*08-bound epitopes and select for widespread viral variation.

Background: It is generally accepted that CD8+ T cell responses play an important role in control of immunodeficiency virus replication. The association of HLA-B27 and -B57 with control of viremia supports this conclusion. However, specific correlates of viral control in individuals expressing these alleles have been difficult to define.

The major histocompatibility complex class II alleles Mamu-DRB1*1003 and -DRB1*0306 are enriched in a cohort of simian immunodeficiency virus-infected rhesus macaque elite controllers.

The role of CD4(+) T cells in the control of human immunodeficiency virus (HIV) and simian immunodeficiency virus (SIV) replication is not well understood. Even though strong HIV- and SIV-specific CD4(+) T-cell responses have been detected in individuals that control viral replication, major histocompatibility complex class II (MHC-II) molecules have not been definitively linked with slow disease progression. In a cohort of 196 SIVmac239-infected Indian rhesus macaques, a group of macaques controlled viral replication to less than 1,000 viral RNA copies/ml.