Evaluation of beneficial and inhibitory effects of nitrate on nodulation and nitrogen fixation in common bean (Phaseolus vulgaris)

AbstractThe effects of applied nitrate on symbiotic nitrogen fixation in legumes are complex. Both inhibition and promotion of nodulation by nitrate have been observed in a dose‐dependent manner. The objectives of this study were to determine the effects of nitrate at different concentrations on root nodulation in different genotypes in common bean (Phaseolus vulgaris). Six genotypes were inoculated with the same rhizobial strain and grown hydroponically in growth pouches in a growth chamber and exposed to six nitrate concentrations, including 0, 2.5, 5, 10, 15, and 20 mM for 4 weeks. The tested genotypes included three recombinant inbred lines (RILs, 25, 46, and 70) that differed in their responses to nitrogen (based on observations of one field growing season), their parents (Mist and Sanilac—registered varieties), which are different in N‐fixing abilities, and one nonnodulating mutant (R99). Our results showed that small amounts of nitrate (2.5 and 5 mM) promoted nodule formation and increased nodule biomass, compared with plants in the 0 nitrate control treatment. In contrast, nitrate concentrations over 10 mM inhibited nodulation, resulting in reductions in nodule number and nodule biomass. Nodulation was completely inhibited by 15‐mM nitrate in all the genotypes. Regression analyses indicated that 5‐mM nitrate is the optimum concentration for promoting nodulation as measured by the total number of nodules formed, the number of effective nodules formed, and the nodule biomass formed. In contrast, nitrogen fixation was inhibited by all levels of nitrate. No genotypic differences were observed in nodulation among the three RILs and their parental cultivars, but all were significantly different than R99, a nonnodulating mutant

The zinc finger protein Zbtb18 represses expression of class I PI3K subunits and inhibits plasma cell differentiation

The PI3K pathway plays a key role in B cell activation and is important for the differentiation of Ab producing plasma cells (PCs). Although much is known about the molecular mechanisms that modulate PI3K signaling in B cells, the transcriptional regulation of PI3K expression is poorly understood. In this study, we identify the zinc finger protein Zbtb18 as a transcriptional repressor that directly binds enhancer/promoter regions of genes encoding class I PI3K regulatory subunits, subsequently limiting their expression, dampening PI3K signaling and suppressing PC responses. Following activation, dividing B cells progressively downregulated Zbtb18, allowing gradual amplification of PI3K signals and enhanced development of PCs. Human Zbtb18 displayed similar expression patterns and function in human B cells, acting to inhibit development of PCs. Furthermore, a number of Zbtb18 mutants identified in cancer patients showed loss of suppressor activity, which was also accompanied by impaired regulation of PI3K genes. Taken together, our study identifies Zbtb18 as a repressor of PC differentiation and reveals its previously unappreciated function as a transcription modulator of the PI3K signaling pathway

Race characterization of <i>Pyrenophora tritici-repentis</i> and sensitivity to propiconazole and pyraclostrobin fungicides

<p>Tan spot, caused by <i>Pyrenophora tritici-repentis</i> (<i>Ptr</i>), is one of the most destructive leaf spot diseases of wheat in Canada. Several races of the fungus are known to occur. Wheat growers have adopted fungicides to manage tan spot; however, intensive spraying may lead to development of reduced sensitivity to fungicides in the pathogen. In this study, 62 <i>Ptr</i> isolates were collected from across Saskatchewan and Alberta and characterized to race on a wheat differential set, with confirmation of race designations by polymerase chain reaction. This same set of isolates, and 27 isolates from an earlier study, were also evaluated for sensitivity to propiconazole and pyraclostrobin fungicides by determining the effective concentration of each needed to inhibit radial growth and conidiospore germination by 50%. Races 1 and 2 were predominant in western Canada, with 57% of isolates classified as race 1 and 40% as race 2. In Alberta, race 1 was most common (76%), while in Saskatchewan, it was race 2 (57%). Two of 26 isolates were classified as race 3, which was detected only in Saskatchewan in 2013. There was no evidence of reduced sensitivity of either fungicide in the <i>Ptr</i> isolates examined. This study provides a baseline for <i>Ptr</i> sensitivity to propiconazole and pyraclostrobin to which future collections of the pathogen may be compared.</p

The zinc finger protein zbtb18 represses expression of class i phosphatidylinositol 3-kinase subunits and inhibits plasma cell differentiation

The PI3K pathway plays a key role in B cell activation and is important for the differentiation of Ab producing plasma cells (PCs). Although much is known about the molecular mechanisms that modulate PI3K signaling in B cells, the transcriptional regulation of PI3K expression is poorly understood. In this study, we identify the zinc finger protein Zbtb18 as a transcriptional repressor that directly binds enhancer/promoter regions of genes encoding class I PI3K regulatory subunits, subsequently limiting their expression, dampening PI3K signaling and suppressing PC responses. Following activation, dividing B cells progressively downregulated Zbtb18, allowing gradual amplification of PI3K signals and enhanced development of PCs. Human Zbtb18 displayed similar expression patterns and function in human B cells, acting to inhibit development of PCs. Furthermore, a number of Zbtb18 mutants identified in cancer patients showed loss of suppressor activity, which was also accompanied by impaired regulation of PI3K genes. Taken together, our study identifies Zbtb18 as a repressor of PC differentiation and reveals its previously unappreciated function as a transcription modulator of the PI3K signaling pathway