Homologous and heterologous desensitization and synergy in pathways leading to the soybean oxidative burst.

Because the H2O2 and O2- generated during a pathogen-triggered oxidative burst could either protect or destroy a besieged plant cell, their synthesis might be expected to be tightly regulated. We have examined the nature of this regulation as it is communicated between homologous and heterologous oxidative-burst pathways, using both chemical (oligogalacturonic acid, harpin, fensulfothion) and mechanical (osmotic stress) stimuli to induce the burst. We report here that the above three chemical elicitors attenuate a subsequent oxidative burst induced in cultured soybean (Glycine max L.

The peroxisome biogenesis disorder group 4 gene, PXAAA1, encodes a cytoplasmic ATPase required for stability of the PTS1 receptor.

In humans, defects in peroxisome assembly result in the peroxisome biogenesis disorders (PBDs), a group of genetically heterogeneous, lethal recessive diseases. We have identified the human gene PXAAA1 based upon its similarity to PpPAS5, a gene required for peroxisome assembly in the yeast Pichia pastoris. Expression of PXAAA1 restored peroxisomal protein import in fibroblasts from 16 unrelated members of complementation group 4 (CG4) of the PBD.

Evidence for a Mechanically Induced Oxidative Burst.

Rapid release of H2O2 may constitute an initial defense response mounted by a plant. Inauguration of this oxidative burst is known to occur upon stimulation with chemical elicitors, but the possibility of mechanical elicitation arising from pathogen penetration/weakening of the cell wall has never been examined. To introduce an adjustable mechanical stress on the plasma membrane, cultured soybean (Glycine max Merr.