Home About us Contact
|
Home About us Contact | ||
|
|
||
Massive Accumulation (massive + accumulation)
Selected AbstractsTowards clarification of the biological role of microcystins, a family of cyanobacterial toxinsENVIRONMENTAL MICROBIOLOGY, Issue 4 2007Daniella Schatz Summary Microcystins constitute a serious threat to the quality of drinking water worldwide. These protein phosphatase inhibitors are formed by various cyanobacterial species, including Microcystis sp. Microcystins are produced by a complex microcystin synthetase, composed of peptide synthetases and polyketide synthases, encoded by the mcyA-J gene cluster. Recent phylogenetic analysis suggested that the microcystin synthetase predated the metazoan lineage, thus dismissing the possibility that microcystins emerged as a means of defence against grazing, and their original biological role is not clear. We show that lysis of Microcystis cells, either mechanically or because of various stress conditions, induced massive accumulation of McyB and enhanced the production of microcystins in the remaining Microcystis cells. A rise in McyB content was also observed following exposure to microcystin or the protease inhibitors micropeptin and microginin, also produced by Microcystis. The extent of the stimulation by cell extract was strongly affected by the age of the treated Microcystis culture. Older cultures, or those recently diluted from stock cultures, hardly responded to the components in the cell extract. We propose that lysis of a fraction of the Microcystis population is sensed by the rest of the cells because of the release of non-ribosomal peptides. The remaining cells respond by raising their ability to produce microcystins thereby enhancing their fitness in their ecological niche, because of their toxicity. [source] Masses of phosphorylated neurofilaments are associated with abnormal Golgi apparatus of anterior horn neurons of ,, ,,-iminodipropionitrile-intoxicated ratsNEUROPATHOLOGY, Issue 2 2002Makoto Uesugi The Golgi apparatus (GA) of anterior horn neurons of rats chronically intoxicated with ,,,,-iminodipropionitrile (IDPN) in drinking water was examined with an organelle-specific antibody. The neuropile of the anterior horns contained the typical axonal spheroids associated with IDPN toxicity while the perikarya of approximately one-third of the neurons contained phosphorylated neurofilaments, which are not found in the perikarya of control rat neurons. By serial or double immunostaining with the SMI-31 and anti-MG 160 antibodies, there were no morphological changes of the GA in the majority of neurons including neurons with a mild to moderate degree of neurofilamentous accumulation. However, a few neurons with a massive accumulation of phosphorylated neurofilaments contained abnormal profiles of the GA which consisted of focal clustering, reduction in size and fragmentation. The results suggest that masses of phosphorylated neurofilaments are associated with struc-tural abnormalities of the GA. [source] Role of hydrogen peroxide during the interaction between the hemibiotrophic fungal pathogen Septoria tritici and wheatNEW PHYTOLOGIST, Issue 3 2007Nandini P. Shetty Summary ,,Hydrogen peroxide (H2O2) is reported to inhibit biotrophic but benefit necrotrophic pathogens. Infection by necrotrophs can result in a massive accumulation of H2O2 in hosts. Little is known of how pathogens with both growth types are affected (hemibiotrophs). The hemibiotroph, Septoria tritici, infecting wheat (Triticum aestivum) is inhibited by H2O2 during the biotrophic phase, but a large H2O2 accumulation occurs in the host during reproduction. ,,Here, we infiltrated catalase, H2O2 or water into wheat during the biotrophic or the necrotrophic phase of S. tritici and studied the effect of infection on host physiology to get an understanding of the survival strategy of the pathogen. ,,H2O2 removal by catalase at both early and late stages made plants more susceptible, whereas H2O2 made them more resistant. H2O2 is harmful to S. tritici throughout its life cycle, but it can be tolerated. ,,The late accumulation of H2O2 is unlikely to result from down-regulation of photosynthesis, but probably originates from damage to the peroxisomes during the general tissue collapse, which is accompanied by release of soluble sugars in a susceptible cultivar. [source] A mass spectrometric strategy for profiling glycoproteinoses, Pompe disease, and sialic acid storage diseasesPROTEOMICS - CLINICAL APPLICATIONS, Issue 4 2008Valegh Faid Abstract Glycoproteinoses, Pompe disease, and sialic acid storage diseases are characterized by a massive accumulation of unprocessed oligosaccharides and/or glycoconjugates in urine. The identification of these glycocompounds is essential for a proper diagnosis. In this study, we investigated the potential of MALDI-TOF-MS to identify glycocompounds present in urine from patients with different inborn errors of glycan metabolism. Urinary glycocompounds were permethylated, and analyzed using GC-MS and MALDI-TOF-MS. In order to confirm tentative assignments, a second aliquot of urine was purified on a C18 Sep-Pak cartridge and glycocompounds were desalted on a column of nonporous graphitized carbon. The glycocompounds were then sequentially on-plate digested using an array of exoglycosidases. A range of disease-specific oligosaccharides as well as glycopeptides was identified for all oligosacchariduria models. In addition, free sialic acid accumulated in urine from a patient suffering from French-type sialuria, has been detected by a GC-MS approach, which could be applied to other sialic acid storage diseases. This procedure is simple, and can be performed in few simple steps in less than 24,h. This current method can be applied for newborn screening for other inherited metabolic diseases as well as for assessing treatments in clinical trials. [source] Spatio-temporal expression of patatin-like lipid acyl hydrolases and accumulation of jasmonates in elicitor-treated tobacco leaves are not affected by endogenous levels of salicylic acidTHE PLANT JOURNAL, Issue 5 2002Sandrine Dhondt Summary We have previously isolated three tobacco genes (NtPat) encoding patatin-like proteins, getting rapidly induced during the hypersensitive response (HR) to tobacco mosaic virus, in advance to jasmonate accumulation. NtPAT enzymes are lipid acyl hydrolases that display high phospholipase A2 (PLA2) activity and may mobilize fatty acid precursors of oxylipins. Here, we performed a detailed study of NtPat gene regulation under various biotic and abiotic stresses. PLA2 activity was poorly induced in response to drought, wounding, reactive oxygen intermediates, salicylic acid (SA) or methyl-jasmonate (MJ) whereas the ethylene (ET) precursor, 1-aminocyclopropane-1-carboxylic acid (ACC), provoked a moderate induction. In contrast, PLA2 activity was strongly induced when ACC was combined with MJ, and in response to the bacterium Erwinia carotovora or to the fungus Botrytis cinerea, as well as to treatment with ,-megaspermin, a cell death-inducing protein elicitor. A simplified system based on the infiltration of ,-megaspermin into leaves was used to dissect the spatio-temporal activation of PLA2 activity with regards to the accumulation of jasmonates and to the influence of endogenous SA. NtPat -encoded PLA2 activity was rapidly induced in the infiltrated zone before the appearance of cell death and with some delay in the surrounding living cells. A massive accumulation of 12-oxo-phytodienoic and jasmonic acids occurred in the elicitor-infiltrated zone, but only low levels were detectable outside this area. A similar picture was found in SA-deficient plants, showing that in tobacco, accumulation of jasmonates is not affected by the concomitant HR-induced build-up of endogenous SA. Finally, ET-insensitive plants showed a weakened induction of PLA2 activity outside the elicitor-infiltrated tissue. [source] Cappuccino mutation in an autoimmune-prone strain of mice suggests a role of platelet function in the progression of immune complex crescentic glomerulonephritisARTHRITIS & RHEUMATISM, Issue 9 2006Minako Yoshida Objective Crescent formation in the renal glomerulus is a typical manifestation of progressive glomerulopathy associated with fatal renal failure; therefore, its prevention is of clinical importance. Little is known about the pathogenic mechanism for crescent formation. This study was undertaken in an attempt to identify the events that are critical for crescent formation in immune complex crescentic glomerulonephritis (CGN) by analyzing a novel mutant strain of mice. Methods A spontaneous mutant strain of mice was isolated from the autoimmune-prone strain EOD, which stably develops fatal CGN. The mutant phenotypes were assessed histopathologically, hematologically, and immunologically. The mutation was searched for with positional cloning using microsatellite markers. Results Compared with wild-type EOD (WT-EOD) mice, mutant EOD (mut-EOD) mice showed marked improvement in CGN in conjunction with an improvement in spontaneous mortality. In WT-EOD mice, an inverse correlation between blood urea nitrogen concentration and blood platelet count and massive accumulation of platelets in the glomerulus were evident, suggesting that an accumulation of platelets in the glomerulus contributes to the progression of CGN. The mutant platelets showed an abnormal aggregation in response to collagen and thrombin, associated with a bleeding tendency in mut-EOD mice. Genetic analysis revealed a deleterious mutation in the cappuccino gene (cno), which encodes a protein that belongs to a complex called the biogenesis of lysosome-related organelle complex 1 and is profoundly involved in platelet function. Morphologic examination revealed a partial defect in dense body formation in the ,-granule of platelets. Conclusion The present findings suggest that platelet functions have a critical role in crescent formation in autoimmune GN. [source] | |||||||||||||