contributed equally to this work.
Conflict of interest:The authors have declared that no conflict of interest exists. Nonstandard abbreviations used: TNF-related apoptosisinducing ligand (TRAIL); death receptor 5 (DR5); concanavalin A (Con-A); mononuclear cell (MNC); alanine aminotransferase (ALT); aspartate aminotransferase (AST).
SUMMARYUsing a high throughput gene microarray technology that detects $22 000 genes, we found that arginase I was the most signi®cantly up-regulated gene in the murine spinal cord during experimental autoimmune encephalomyelitis (EAE). By Northern blot and arginase enzyme assay, we detected high levels of arginase I mRNA and protein, respectively, in the spinal cord of EAE mice, but not in the spinal cord of normal mice or mice that had recovered from EAE. In vitro, both microglia and astrocytes produced arginase and nitric oxide synthase, two enzymes that are involved in arginine metabolism. To explore the roles of arginase in EAE, we injected the arginase inhibitor amino-6-boronohexanoic acid (ABH) into mice during the inductive and effector phases of the disease. Compared with mice that received vehicle control, mice treated with ABH developed milder EAE with delayed onset, reduced disease score and expedited recovery. Spleen mononuclear cells from ABH-treated mice produced more nitric oxide and secreted less interferon-g and tumour necrosis factor-a as compared to control mice. These results indicate that arginase plays important roles in autoimmune in¯ammation in the central nervous system.
Arabidopsis thaliana CEL1 protein was detected in young expanding tissues. Immunostaining revealed that CEL1 accumulated mostly in xylem cells. The primary, as well as the secondary xylem showed considerable CEL1 staining. CEL1 was also observed in young epidermal cells, in which the thicker lateral and tangential walls stained more intensely than the inner walls. In newly formed cell walls, the lateral tangential walls were labeled more intensively than the inner walls. Cellulase activity was found to be significantly higher in growing tissue compared to mature parts of the plant. Cel1 expression concurrently with cellulase activity could be restored in detached matured leaves by sucrose treatment after 48 h in the culture medium.
SUMMARY Transgenic tobacco and Arabidopsis thaliana carrying the Arabidopsis endo-1,4-beta-glucanase (EC 3.2.1.4) Cel1 promoter fused to the beta-glucuronidase (GUS) reporter gene were infected with the root-knot nematode, Meloidogyne incognita, and either the tobacco cyst nematode, Globodera tabacum (tobacco), or beet cyst nematode, Heterodera schachtii (Arabidopsis). Cel1-driven GUS expression was detected in cell elongation zones of noninfected plants and within feeding sites (giant-cells) induced in roots of both plant hosts by M. incognita. The first detectable signs of Cel1 expression within developing giant-cells occurred at the onset of giant-cell formation and continued throughout the M. incognita life cycle. UidA (Gus) transcripts were detectable within giant-cells induced in tobacco roots at 11-13 days postinoculation with M. incognita as determined by in situ mRNA hybridization. By contrast, expression of the Cel1 promoter was not detected within developing syncytia induced in tobacco or Arabidopsis roots by G. tabacum and H. schachtii, respectively, at any time point. The results demonstrate specific regulation of cell wall-degrading enzymes that may be required for cell wall modifications during feeding cell formation by sedentary endoparasitic nematodes. Differential expression of Cel1 by cyst and root-knot nematodes further supports underlying mechanistic differences in giant-cell and syncytium formation.
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