Mapping and validation of quantitative trait loci for resistance to Cercospora zeae-maydis infection in tropical maize (Zea mays L.).

Breeding for resistance to gray leaf spot, caused by Cercospora zeae-maydis (Cz) is paramount for many maize environments, in particular under warm and humid growing conditions. In this study, we mapped and characterized quantitative trait loci (QTL) involved in the resistance of maize against Cz. We confirmed the impact of the QTL on disease severity using near-isogenic lines (NILs), and estimated their effects on three major agronomic traits using their respective near isogenic hybrids (NIHs), which we obtained by crossing the NILs with an inbred from a complementary heterotic pool. We further validated three of the four QTL that were mapped using the Multiple Interval Mapping approach and showed LOD values>2.5. NILs genotype included all combinations between favorable alleles of the two QTL located in chromosome 1 (Q1 in bin 1.05 and Q2 in bin 1.07), and the allele in chromosome 3 (Q3 in bin 3.07). Each of the three QTL separately significantly reduced the severity of Cz. However, we found an unfavorable epistatic interaction between Q1 and Q2: presence of the favorable allele at one of the QTL allele effectively nullified the effect of the favorable allele at the other. In contrast, the interaction between Q2 and Q3 was additive, promoting the reduction of the severity to a greater extent than the sum of their individual effects. When evaluating the NIH we found significant individual effects for Q1 and Q3 on gray leaf spot severity, for Q2 on stalk lodging and grain yield, and for Q3 on grain moisture and stalk lodging. We detected significant epitasis between Q1 and Q2 for grain moisture and between Q1 and Q3 for stalk lodging. These results suggest that the combination of QTL impacts the effectiveness of marker-assisted selection procedures in commercial product development programs.

Involvement of a Salmonella genomic island 1 gene in the rumen protozoan-mediated enhancement of invasion for multiple-antibiotic-resistant Salmonella enterica serovar Typhimurium.

Multiple-antibiotic-resistant Salmonella enterica serotype Typhimurium is a food-borne pathogen that may be more virulent than related strains lacking the multiresistance phenotype. Salmonella enterica serotype Typhimurium phage type DT104 is the most prevalent of these multiresistant/hypervirulent strains. Multiresistance in DT104 is conferred by an integron structure, designated Salmonella genomic island 1 (SGI1), while we recently demonstrated DT104 hyperinvasion mediated by rumen protozoa (RPz) that are normal flora of cattle. Hyperinvasion was also observed in other Salmonella strains, i.e., other S. enterica serovar Typhimurium phage types and other S. enterica serovars, like S. enterica serovar Infantis, possessing SGI1, while DT104 strains lacking SGI1 were not hyperinvasive. Herein we attempted to identify SGI1 genes involved in the RPz-mediated hyperinvasion of Salmonella strains bearing SGI1. Transposon mutagenesis, coupled with a novel reporter system, revealed the involvement of an SGI1 gene previously designated SO13. Disruption of SO13 expression led to an abrogation of hyperinvasion as assessed by tissue culture invasion assays and by bovine challenge experiments. However, hyperinvasion was not observed in non-SGI1-bearing strains of Salmonella engineered to express SO13. That is, SO13 and another SGI1 gene(s) may coordinately upregulate invasion in DT104 exposed to RPz.

The genome of deep-sea vent chemolithoautotroph Thiomicrospira crunogena XCL-2.

Presented here is the complete genome sequence of Thiomicrospira crunogena XCL-2, representative of ubiquitous chemolithoautotrophic sulfur-oxidizing bacteria isolated from deep-sea hydrothermal vents. This gammaproteobacterium has a single chromosome (2,427,734 base pairs), and its genome illustrates many of the adaptations that have enabled it to thrive at vents globally. It has 14 methyl-accepting chemotaxis protein genes, including four that may assist in positioning it in the redoxcline. A relative abundance of coding sequences (CDSs) encoding regulatory proteins likely control the expression of genes encoding carboxysomes, multiple dissolved inorganic nitrogen and phosphate transporters, as well as a phosphonate operon, which provide this species with a variety of options for acquiring these substrates from the environment. Thiom. crunogena XCL-2 is unusual among obligate sulfur-oxidizing bacteria in relying on the Sox system for the oxidation of reduced sulfur compounds. The genome has characteristics consistent with an obligately chemolithoautotrophic lifestyle, including few transporters predicted to have organic allocrits, and Calvin-Benson-Bassham cycle CDSs scattered throughout the genome.

Exposure to rumen protozoa leads to enhancement of pathogenicity of and invasion by multiple-antibiotic-resistant Salmonella enterica bearing SGI1.

Multiple-antibiotic-resistant Salmonella enterica serotype Typhimurium is a food-borne pathogen that has been purported to be more virulent than antibiotic-sensitive counterparts. The paradigm for this multiresistant/hyperpathogenic phenotype is Salmonella enterica serotype Typhimurium phage type DT104 (DT104). The basis for the multiresistance in DT104 is related to an integron structure designated SGI1, but factors underlying hyperpathogenicity have not been completely identified. Since protozoa have been implicated in the alteration of virulence in Legionella and Mycobacterium spp., we attempted to assess the possibility that protozoa may contribute to the putative hypervirulence of DT104. Our study reveals that DT104 can be more invasive, as determined by a tissue culture invasion assay, after surviving within protozoa originating from the bovine rumen. The enhancement of invasion was correlated with hypervirulence in a bovine infection model in which we observed a more rapid progression of disease and a greater recovery rate for the pathogen. Fewer DT104 cells were recovered from tissues of infected animals when protozoa were lysed by preinfection chemical defaunation of the bovine or ovine rumen. The protozoan-mediated hypervirulence phenotype was observed only in DT104 and other Salmonella strains, including serovars Agona and Infantis, possessing SGI1.

SlyA regulates the collagenase-mediated cytopathic phenotype in multiresistant Salmonella.

Salmonella enterica serotype Typhimurium phagetype DT104 (DT104) is a foodborne pathogen with a multiresistant phenotype conferred by a genomic-based integron structure designated as SGI1. Recently, a novel cytopathic phenotype was ascribed to several isolates of DT104 recovered from veal calves. This phenotype is dependent upon clg, a gene encoding a collagenase in Salmonella. Using a novel transposon system and an RT-PCR assay for detection of clg expression, we identified SlyA as a regulator of the collagenase-mediated phenotype. The function of SlyA, in regards to clg expression, is to repress the synthesis of Clg. Derepression ensued in the absence of SlyA or in the presence of a truncated version of SlyA with the latter being relevant for maintenance of another virulence aspect mediated by SlyA, i.e. survival within macrophages. The SlyA-mediated effect on clg expression was restricted to DT104 and other Salmonella phagetypes and serotypes possessing SGI1 thus suggesting co-regulation by an SGI1-specific component.