RsmA is an RNA-binding protein functioning as a global post-transcriptional regulator of various cellular processes in bacteria and has been demonstrated to be an important virulence regulator in many animal bacterial pathogens. However, its function in other phytopathogenic bacteria is unclear, except for the Erwinia carotovora RsmA, which acts as a negative virulence regulator. In this work, we investigated the function of the rsmA-like gene, named rsmA(Xcc), of the phytopathogen Xanthomonas campestris pv. campestris. Deletion of rsmA(Xcc) resulted in complete loss of virulence on the host plant Chinese radish, hypersensitive response on the nonhost plant pepper ECW-10R, and motility on the surface of an agar plate. The rsmA(Xcc) mutant displayed a significant reduction in the production of extracellular amylase, endoglucanase, and polysaccharide, but a significant increase in intracellular glycogen accumulation and an enhanced bacterial aggregation and cell adhesion. Microarray hybridization and semiquantitative reverse-transcription polymerase chain reaction analysis showed that deletion of rsmA(Xcc) led to significantly reduced expression of genes encoding the type III secretion system (T3SS), T3SS-effectors, and the bacterial aggregate dispersing enzyme endo-beta-1,4-mannanase. These results suggest that rsmA(Xcc) is involved in the control of various cellular processes, including pathogenesis of X. campestris pv. campestris.
The MarR family of transcriptional regulators of bacteria are involved in the regulation of many cellular processes, including pathogenesis. In this work, we have demonstrated genetically that hpaR (hpa, hrp associated), which encodes a putative MarR family regulator, is involved in the hypersensitive response (HR), pathogenicity, and extracellular protease production of the phytopathogenic bacterium Xanthomonas campestris pathovar campestris. A mutation in hpaR resulted in complete loss of virulence in the host plant cabbage, a delayed and weakened HR in the nonhost plant pepper ECW-10R, and an increase in extracellular protease production. Detection of the -glucuronidase activity of a plasmid-driven hpaR promoter-gusA reporter revealed that the expression of hpaR is positively controlled by HrpG and HrpX and is suppressed in rich medium while being strongly induced in minimal and hrp-inducing media and inside the host. These findings indicate that hpaR belongs to the hrpG and hrpX regulon and that HrpX regulates the extracellular protease production via hpaR in X. campestris pv. campestris.
The data suggest that propofol alleviated ECS-induced learning-memory impairment without interfering with the antidepressant efficacy of ECS, possibly by inhibiting excessive expression of GAD65 and maintaining the balance between glutamatergic and GABAergic amino acids neurotransmitters in the hippocampus.
The glutamate content in hippocampus of depressed rats heightens, and the NMDA-NR2B expression down-regulated, which may cause "depression" symptoms and learning memory impairment. After ECT, the glutamate contents decreased, and NMDA-NR2B expression up-regulated, the depression symptoms improved, and the spatial memory worsened simultaneously. However, propofol inhibited the excessive decrease of glutamate and excessive up-regulation of NMDA-NR2B caused by ECT, and both the depression symptoms and the spatial memory of depressed rats improved.
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