Composition and Distribution of Free Amino Acids in Flatpea (Lathyrus sylvestris L.) as Influenced by Water Deficit and Plant Age

Drought-stressed flatpea (Lathyrus sylvestris L.) plants from8 to 22 weeks old were analysed for nitrogen, soluble proteinand free amino acids. An increase in nitrogen and free aminoacid concentrations and a decrease in soluble protein levelwere observed in roots of plants up to 16 weeks old. The cumulativeconcentration of free amino acids increased with drought stress.Tissue concentrations of 2, 4-diaminobutyric acid (1.6–2.6%of the dry weight) were highest in leaves. Levels increasedsteadily, nearly doubling, in leaves and stems between weeks10 and 16. Levels in drought-stressed leaves were, on average,11.9% higher than those of controls. Estimated concentrationsof a mixture of 4-aminobutyric acid and an unknown amino acidwere highest in stems, increased in this tissue with age andtended to increase in stems and leaves and decrease in rootsin response to water deficit. Levels of the mixture of homoserineand another unidentified amino acid were not influenced by ageor water status of the plants. Root concentrations of asparagine,arginine, glutamine, aspartate, and another prominent, unidentifiedamino acid increased with plant age and reached a peak at thetime of flowering (14 to 18 weeks). Only the concentration ofthe unknown compound was elevated following drought stress.Concentrations of valine, isoleucine, leucine, phenylalanine,and methionine also increased during this period and were elevatedin drought-stressed plants. Proline levels increased with plantage and drought stress, but proline accounted for only about10% of the total free amino acids in the drought-stressed plants. Key words: 2, 4-Diaminobutyric acid, drought, flatpea     

Ferricrocin synthesis in Magnaporthe grisea and its role in pathogenicity in rice

Iron is an essential element for the growth of nearly all organisms. In order to overcome the problem of its low bioavailability, microorganisms (including fungi) secrete siderophores, high-affinity iron chelators. As the acquisition of iron is also a key step in infection processes, siderophores have been considered as potential virulence factors in several host–pathogen interactions. Most fungi produce siderophores of the hydroxamate-type, which are synthesized by non-ribosomal peptide synthetases (NRPSs). Magnaporthe grisea , the causal agent of rice blast disease, produces ferricrocin as intracellular storage siderophore and excretes coprogens. In the M. grisea genome we identified SSM1 , an NRPS gene, and a gene encoding an l -ornithine N5-monooxygenase ( OMO1 ) that is clustered with SSM1 and responsible for catalysing the first step in siderophore biosynthesis, the N⁵ hydroxylation of ornithine. Disruption of SSM1 confirmed that the gene encodes ferricrocin synthetase. Pathogenicity of these mutants towards rice was reduced, suggesting a role of this siderophore in pathogenicity of M. grisea .     

<Emphasis Type="Italic">TRAF1/C5</Emphasis>polymorphism is not associated with increased mortality in rheumatoid arthritis: two large longitudinal studies

Introduction  

Recently an association between a genetic variation in TRAF1/C5 and mortality from sepsis or cancer was found in rheumatoid arthritis (RA). The most prevalent cause of death, cardiovascular disease, may have been missed in that study, since patients were enrolled at an advanced disease stage. Therefore, we used an inception cohort of RA patients to investigate the association between TRAF1/C5 and cardiovascular mortality, and replicate the findings on all-cause mortality. As TRAF1/C5 associated mortality may not be restricted to RA, we also studied a large cohort of non-RA patients.     

Mesenchymal stem cells in autoimmune diseases: hype or hope?

Intervention with mesenchymal stem cells (MSCs) represents a promising therapeutic tool in treatment-refractory autoimmune diseases. A new report by Schurgers and colleagues in a previous issue of Arthritis Research & Therapy sheds novel mechanistic insight into the pathways employed by MSCs to suppress T-cell proliferation in vitro, but, at the same time, indicates that MSCs do not influence T-cell reactivity and the disease course in an in vivo arthritis model. Such discrepancies between the in vitro and in vivo effects of potent cellular immune modulators should spark further research and should be interpreted as a sign of caution for the in vitro design of MSC-derived interventions in the setting of human autoimmune diseases.