Genome-wide association mapping for resistance to bacterial blight and bacterial leaf streak in rice.

MAIN CONCLUSION: Using genome-wide SNP association mapping, a total of 77 and 7 loci were identified for rice bacterial blight and bacterial leaf streak resistance, respectively, which may facilitate rice resistance improvement. Bacterial blight (BB) and bacterial leaf streak (BLS) caused by Gram-negative bacteria Xanthomonas oryzae pv. oryzae (Xoo) and X. oryzae pv. oryzicola (Xoc), respectively, are two economically important diseases negatively affecting rice production. To mine new sources of resistance, a set of rice germplasm collection consisting of 895 re-sequenced accessions from the 3000 Rice Genomes Project (3 K RGP) were screened for BB and BLS resistance under field conditions. Higher levels of BB resistance were observed in aus/boro subgroup, whereas the japonica, temperate japonica and tropical japonica subgroups possessed comparatively high levels of resistance to BLS. A genome-wide association study (GWAS) mined 77 genomic loci significantly associated with BB and 7 with BLS resistance. The phenotypic variance (R2) explained by these loci ranged from 0.4 to 30.2%. Among the loci, 7 for BB resistance were co-localized with known BB resistance genes and one for BLS resistance overlapped with a previously reported BLS resistance QTL. A search for the candidates in other novel loci revealed several defense-related genes that may be involved in resistance to BB and BLS. High levels of phenotypic resistance to BB or BLS could be attributed to the accumulation of the resistance (R) alleles at the associated loci, indicating their potential value in rice resistance breeding via gene pyramiding. The GWAS analysis validated the known genes underlying BB and BLS resistance and identified novel loci that could enrich the current resistance gene pool. The resources with strong resistance and significant SNPs identified in this study are potentially useful in breeding for BB and BLS resistance.

Genomics-Assisted Improvement of Super High-Yield Hybrid Rice Variety "Super 1000" for Resistance to Bacterial Blight and Blast Diseases.

The two-line rice hybrid "Super 1000" (GX24S × R900) represents a major landmark achievement of breeding for super-hybrid rice in China. However, both male parent R900 and hybrid "Super 1000" have an obvious defect of high susceptibility to rice bacterial blight (BB) and blast. Thus, improving disease resistance and maintaining the original high-yield capacity are essential for the sustainable application of "Super 1000." In this study, the application of closely linked single-nucleotide polymorphism (SNP) markers for foreground selection of dominant resistance gene loci together with genome-wide SNP markers for the background selection rapidly improved the disease resistance of R900 without disturbing its high-yield capacity. A series of improved R900 lines (iR900, in BC2Fn and BC3Fn generations) were developed to stack resistance genes (Xa23+Pi9, Xa23+Pi1+Pi2/9) by marker-assisted backcrossing and field selection for phenotypes, and further crossed with the female line GX24S to obtain improved hybrid variety Super 1000 (iS1000). The genetic backgrounds of iS1000 and "Super 1000" were profiled by using a 56 K SNP-Chip, and results showed that they shared 98.76% of similarity. Meanwhile, evaluation of the field disease resistance showed that the iR900 lines and iS1000 hybrids possess significantly enhanced resistance to both BB and rice blast. Resistance spectrum assays revealed that the iR900 lines and their derived hybrids exhibited high-level resistance to 28 Xoo strains tested, and enhanced resistance to leaf blast at the seedling stage when infected with 38 Magnaporthe oryzae isolates. Between 2019 and 2020, the multi-location field trials across the middle and lower reaches of the Yangtze River were launched and showed that the iS1000 slightly out-yielded than the original variety. In a large-scale demonstration site (6.73 ha, Yunnan, China), the iS1000 achieved 17.06 t/hm2 of yield in 2019. Moreover, the high similarity was observed in main agronomic traits and grain quality when comparing the improved lines/hybrids to original ones (iR900 vs. R900, iS1000 vs. S1000). This work presented a typical genomics-assisted breeding strategy and practice, which involves in directional introgression and rapid stack of multiple disease resistance genes, endowing the super-high-yield hybrid rice variety with holistic disease resistance but without yield penalty.

Both hematopoietic-derived and non-hematopoietic-derived {beta}-arrestin-2 regulates murine allergic airway disease.

Allergic asthma, a major cause of morbidity and leading cause of hospitalizations, is an inflammatory disease orchestrated by T helper cells and characterized by the lung migration of eosinophils, which are important asthma effector cells. Lung migration of inflammatory cells requires, among other events, the chemokine receptor transduction of lung-produced inflammatory chemokines. Despite the widespread prevalence of this disease, the molecular mechanisms regulating chemokine production and receptor regulation in asthma are poorly understood. Previous work from our laboratory demonstrated that beta-arrestin-2 positively regulates the development of allergic airway disease in a mouse model, partly through positive regulation of T-lymphocyte chemotaxis to the lung. However, beta-arrestin-2 is expressed in many cell types, including other hematopoietic cells and lung structural cells, which are involved in the development and manifestation of allergic airway disease. To determine the cell types required for beta-arrestin-2-dependent allergic inflammation, we generated bone marrow chimera mice. Using the ovalbumin murine model of allergic airway disease, we show that eosinophilic and lymphocytic inflammation is restored in chimeric mice, with expression of beta-arrestin-2 exclusively on hematopoietic-derived cell types. In contrast, airway hyperresponsiveness is dependent on the expression of beta-arrestin-2 in structural cells. Our data demonstrate that the expression of beta-arrestin-2 in at least two divergent cell types contributes to the pathogenesis of allergic airway disease.

Chronic LPS inhalation causes emphysema-like changes in mouse lung that are associated with apoptosis.

Lipopolysaccharide (LPS) is ubiquitous in the environment. Recent epidemiologic data suggest that occupational exposure to inhaled LPS can contribute to the progression of chronic obstructive pulmonary disease. To address the hypothesis that inhaled LPS can cause emphysema-like changes in mouse pulmonary parenchyma, we exposed C57BL/6 mice to aerosolized LPS daily for 4 weeks. By 3 days after the end of the 4-week exposure, LPS-exposed mice developed enlarged airspaces that persisted in the 4-week recovered mice. These architectural alterations in the lung are associated with enhanced type I, III, and IV procollagen mRNA as well as elevated levels of matrix metalloproteinase (MMP)-9 mRNA, all of which have been previously associated with human emphysema. Interestingly, MMP-9-deficient mice were not protected from the development of LPS-induced emphysema. However, we demonstrate that LPS-induced airspace enlargement was associated with apoptosis within the lung parenchyma, as shown by prominent TUNEL staining and elevated cleaved caspase 3 immunoreactivity. Antineutrophil antiserum-treated mice were partially protected from the lung destruction caused by chronic inhalation of LPS. Taken together, these findings demonstrate that inhaled LPS can cause neutrophil-dependent emphysematous changes in lung architecture that are associated with apoptosis and that these changes may be occurring through mechanisms different than those induced by cigarette smoke.