The Hfq protein is reported to be an RNA chaperone, which is involved in the stress response and the virulence of several pathogens. In E. coli, Hfq can mediate the interaction between some sRNAs and their target mRNAs. But it is controversial whether Hfq plays an important role in S. aureus. In this study, we found that the deletion of hfq gene in S. aureus 8325-4 can increase the surface carotenoid pigments. The hfq mutant was more resistant to oxidative stress but the pathogenicity of the mutant was reduced. We reveal that the Hfq protein can be detected only in some S. aureus strains. Using microarray and qRT-PCR, we identified 116 genes in the hfq mutant which had differential expression from the wild type, most of which are related to the phenotype and virulence of S. aureus. Among the 116 genes, 49 mRNAs can specifically bind Hfq protein, which indicates that Hfq also acts as an RNA binding protein in S. aureus. Our data suggest that Hfq protein of S. aureus is a multifunctional regulator involved in stress and virulence.

Fusarium ear rot (FER) incited by Fusarium verticillioides is a major disease of maize that reduces grain quality globally. Host resistance is the most suitable strategy for managing the disease. We report the results of genome-wide association study (GWAS) to detect alleles associated with increased resistance to FER in a set of 818 tropical maize inbred lines evaluated in three environments. Association tests performed using 43,424 single-nucleotide polymorphic (SNPs) markers identified 45 SNPs and 15 haplotypes that were significantly associated with FER resistance. Each associated SNP locus had relatively small additive effects on disease resistance and accounted for 1–4% of trait variation. These SNPs and haplotypes were located within or adjacent to 38 candidate genes, 21 of which were candidate genes associated with plant tolerance to stresses, including disease resistance. Linkage mapping in four biparental populations to validate GWAS results identified 15 quantitative trait loci (QTL) associated with F. verticillioides resistance. Integration of GWAS and QTL to the maize physical map showed eight colocated loci on chromosomes 2, 3, 4, 5, 9, and 10. QTL on chromosomes 2 and 9 are new. These results reveal that FER resistance is a complex trait that is conditioned by multiple genes with minor effects. The value of selection on identified markers for improving FER resistance is limited; rather, selection to combine small effect resistance alleles combined with genomic selection for polygenic background for both the target and general adaptation traits might be fruitful for increasing FER resistance in maize.

BackgroundCommon rust, caused by Puccinia sorghi, is an important foliar disease of maize that has been associated with up to 50% grain yield loss. Development of resistant maize germplasm is the ideal strategy to combat P. sorghi.ResultsAssociation mapping performed using a mixed linear model (MLM), integrating population structure and family relatedness identified 25 QTL (P < 3.12 × 10− 5) that were associated with resistance to common rust and distributed on chromosomes 1, 3, 5, 6, 8, and 10. We identified three QTLs associated with all three disease parameters (final disease rating, mean disease rating, and area under disease progress curve) located on chromosomes 1, 3, and 8. A total of 5 QTLs for resistance to common rust were identified in the RIL population. Nine candidate genes located on chromosomes 1, 5, 6, 8, and 10 for resistance to common rust associated loci were identified through detailed annotation.ConclusionsUsing a diverse set of inbred lines genotyped with high density markers and evaluated for common rust resistance in multiple environments, it was possible to identify QTL significantly associated with resistance to common rust and several candidate genes. The results point to the need for fine mapping common rust resistance by targeting regions identified in common between this study and others using diverse germplasm.Electronic supplementary materialThe online version of this article (10.1186/s12870-018-1520-1) contains supplementary material, which is available to authorized users.