Plant defenses against pathogens and insects are regulated differentially by cross-communicating signal transduction pathways in which salicylic acid (SA) and jasmonic acid (JA) play key roles. In this study, we investigated the molecular mechanism of the antagonistic effect of SA on JA signaling. Arabidopsis plants unable to accumulate SA produced 25-fold higher levels of JA and showed enhanced expression of the JA-responsive genes LOX2 , PDF1.2 , and VSP in response to infection by Pseudomonas syringae pv tomato DC3000, indicating that in wild-type plants, pathogen-induced SA accumulation is associated with the suppression of JA signaling. Analysis of the Arabidopsis mutant npr1 , which is impaired in SA signal transduction, revealed that the antagonistic effect of SA on JA signaling requires the regulatory protein NPR1. Nuclear localization of NPR1, which is essential for SA-mediated defense gene expression, is not required for the suppression of JA signaling, indicating that cross-talk between SA and JA is modulated through a novel function of NPR1 in the cytosol.

Hydrochory, or the passive dispersal of organisms by water, is an important means of propagule transport, especially for plants. During recent years, knowledge about hydrochory and its ecological consequences has increased considerably and a substantial body of literature has been produced. Here, we review this literature and define the state of the art of the discipline. A substantial proportion of species growing in or near water have propagules (fruits, seeds or vegetative units) able to disperse by water, either floating, submerged in flowing water, or with the help of floating vessels. Hydrochory can enable plants to colonize sites out of reach with other dispersal vectors, but the timing of dispersal and mechanisms of establishment are important for successful establishment. At the population level, hydrochory may increase the effective size and longevity of populations, and control their spatial configuration. Hydrochory is also an important source of species colonizing recruitment-limited riparian and wetland communities, contributing to maintenance of community species richness. Dispersal by water may even influence community composition in different landscape elements, resulting in landscape-level patterns. Genetically, hydrochory may reduce spatial aggregation of genetically related individuals, lead to high gene flow among populations, and increase genetic diversity in populations receiving many propagules. Humans have impacted hydrochory in many ways. For example, dams affect hydrochory by reducing peak flows and hence dispersal capacity, altering the timing of dispersal, and by presenting physical barriers to dispersal, with consequences for riverine plant communities. Hydrochory has been inferred to be an important vector for the spread of many invasive species, but there is also the potential for enhancing ecosystem restoration by improving or restoring water dispersal pathways. Climate change may alter the role of hydrochory by modifying the hydrology of water-bodies as well as conditions for propagule release and plant colonization.

IgA nephropathy (IgAN) is characterized by circulating immune complexes composed of galactose-deficientIgA1 and a glycan-specific IgG antibody. These immune complexes deposit in the glomerular mesangium and induce the mesangioproliferative glomerulonephritis characteristic of IgAN. To define the precise specificities and molecular properties of the IgG antibodies, we generated EBV-immortalized IgG-secreting lymphocytes from patients with IgAN and found that the secreted IgG formed complexes with galactose-deficient IgA1 in a glycan-dependent manner. We cloned and sequenced the heavy-and light-chain antigen-binding domains of IgG specific for galactose-deficient IgA1 and identified an A to S substitution in the complementarity-determining region 3 of the variable region of the gene encoding the IgG heavy chain in IgAN patients. Furthermore, site-directed mutagenesis that reverted the residue to alanine reduced the binding of recombinant IgG to galactose-deficient IgA1. Finally, we developed a dot-blot assay for the glycan-specific IgG antibody that differentiated patients with IgAN from healthy and disease controls with 88% specificity and 95% sensitivity and found that elevated levels of this antibody in the sera of patients with IgAN correlated with proteinuria. Collectively, these findings indicate that glycan-specific antibodies are associated with the development of IgAN and may represent a disease-specific marker and potential therapeutic target.

Aberrant glycosylation of IgA1 plays an essential role in the pathogenesis of IgA nephropathy. This abnormality is manifested by a deficiency of galactose in the hinge-region O-linked glycans of IgA1. Biosynthesis of these glycans occurs in a stepwise fashion beginning with the addition of N-acetylgalactosamine by the enzyme N-acetylgalactosaminyltransferase 2 and continuing with the addition of either galactose by β1,3-galactosyltransferase or a terminal sialic acid by a N-acetylgalactosamine-specific α2,6-sialyltransferase. To identify the molecular basis for the aberrant IgA glycosylation, we established EBV-immortalized IgA1-producing cells from peripheral blood cells of patients with IgA nephropathy. The secreted IgA1 was mostly polymeric and had galactose-deficient O-linked glycans, characterized by a terminal or sialylated N-acetylgalactosamine. As controls, we showed that EBV-immortalized cells from patients with lupus nephritis and healthy individuals did not produce IgA with the defective galactosylation pattern. Analysis of the biosynthetic pathways in cloned EBV-immortalized cells from patients with IgA nephropathy indicated a decrease in β1,3-galactosyltransferase activity and an increase in N-acetylgalactosamine-specific α2,6-sialyltransferase activity. Also, expression of β1,3-galactosyltransferase was significantly lower, and that of N-acetylgalactosamine-specific α2,6-sialyltransferase was significantly higher than the expression of these genes in the control cells. Thus, our data suggest that premature sialylation likely contributes to the aberrant IgA1 glycosylation in IgA nephropathy and may represent a new therapeutic target.

We propose that the relationship between diversity and community invasibility depends on the degree to which community composition is driven by immigration processes. When immigration is enhanced by high propagule pressure or low‐intensity disturbance, the relationship between diversity and exotic species invasion should be positive. Only when such immigration processes are limited should competitive interactions lead to a negative correlation between diversity and invasibility. Moreover, competition should be more apparent at smaller scales where individual plants compete directly for space; thus, diversity and invasibility are more likely to be negatively correlated at small spatial scales. We tested these predictions by comparing exotic and native species diversity of vascular plants across five spatial scales in riparian and upland plant communities in the southern Appalachians. We found a positive relationship between species diversity and exotic invasion in riparian areas at large scales (100 m2), which graded into a negative relationship at small scales (0.01 m2). In uplands, there was a slight positive relationship between native and exotic species diversity at both scales of observation. Overall, riparian areas had more exotic and native species than upland areas, and both native and exotic species diversity increased with flood frequency within the riparian zone. Corresponding Editor: T. J. Stohlgren.

The PDF1.2 gene of Arabidopsis encoding a plant defensin is commonly used as a marker for characterization of the jasmonate-dependent defense responses. Here, using PDF1.2 promoter-deletion lines linked to the ␤-glucoronidase-reporter gene, we examined putative promoter elements associated with jasmonate-responsive expression of this gene. Using stably transformed plants, we first characterized the extended promoter region that positively regulates basal expression from the PDF1.2 promoter. Second, using promoter deletion constructs including one from which the GCC-box region was deleted, we observed a substantially lower response to jasmonate than lines carrying this motif. In addition, point mutations introduced into the core GCC-box sequence substantially reduced jasmonate responsiveness, whereas addition of a 20-nucleotide-long promoter element carrying the core GCC-box and flanking nucleotides provided jasmonate responsiveness to a 35S minimal promoter. Taken together, these results indicated that the GCC-box plays a key role in conferring jasmonate responsiveness to the PDF1.2 promoter. However, deletion or specific mutations introduced into the core GCC-box did not completely abolish the jasmonate responsiveness of the promoter, suggesting that the other promoter elements lying downstream from the GCC-box region may also contribute to jasmonate responsiveness. In other experiments, we identified a jasmonate-and pathogen-responsive ethylene response factor transcription factor, AtERF2, which when overexpressed in transgenic Arabidopsis plants activated transcription from the PDF1.2, Thi2.1, and PR4 (basic chitinase) genes, all of which contain a GCC-box sequence in their promoters. Our results suggest that in addition to their roles in regulating ethylene-mediated gene expression, ethylene response factors also appear to play important roles in regulating jasmonate-responsive gene expression, possibly via interaction with the GCC-box.Diseases caused by fungal, bacterial, and viral pathogens result in enormous reductions in yield and quality from agricultural crops around the world. However, although plants are continuously challenged by pathogenic microorganisms, the development of disease is a relatively rare event. It is clear, therefore, that plants possess efficient defense systems. Effective induction of the defense response requires pathogen recognition followed by a network of signal transduction processes, resulting in the rapid activation of defense gene expression. A number of secondary signal molecules such as salicylic acid (SA), jasmonic acid (JA) and its methyl ester, methyl jasmonate (MeJA), and ethylene act to amplify and regulate defense responses after initial activation (Dong, 1998; Reymond and Farmer, 1998; Schenk et al., 2000). Interestingly, the SA-and jasmonate/ethylene-dependent signaling pathways appear to modulate plant defense responses against different classes of pathogens (for review, see Thomma et al., 2001). Treatment with MeJA provides Arabidopsis plants with protection ag...

The microbiota promotes resistance to respiratory infection, but the mechanistic basis for this is poorly defined. Here, we identify members of the microbiota that protect against respiratory infection by the major human pathogens Streptococcus pneumoniae and Klebsiella pneumoniae. We show that the microbiota enhances respiratory defenses via granulocyte–macrophage colony-stimulating factor (GM-CSF) signaling, which stimulates pathogen killing and clearance by alveolar macrophages through extracellular signal-regulated kinase signaling. Increased pulmonary GM-CSF production in response to infection is primed by the microbiota through interleukin-17A. By combining models of commensal colonization in antibiotic-treated and germ-free mice, using cultured commensals from the Actinobacteria, Bacteroidetes, Firmicutes, and Proteobacteria phyla, we found that potent Nod-like receptor-stimulating bacteria in the upper airway (Staphylococcus aureus and Staphylococcus epidermidis) and intestinal microbiota (Lactobacillus reuteri, Enterococcus faecalis, Lactobacillus crispatus and Clostridium orbiscindens) promote resistance to lung infection through Nod2 and GM-CSF. Our data reveal the identity, location, and properties of bacteria within the microbiota that regulate lung immunity, and delineate the host signaling axis they activate to protect against respiratory infection.

Overall, these findings suggest that CIC containing aberrantly glycosylated IgA1 affect proliferation of MC in vitro and, thus, likely play a role in the pathogenesis of IgAN.