The defenses against free radical damage include specialized repair enzymes that correct oxidative damages in DNA, and detoxification systems such as superoxide dismutases. These defenses may be coordinated genetically as global responses. We hypothesized that the expression of the SOD and the DNA repair genes would inhibit DNA damage under oxidative stress. Therefore, the protection of E. coli mutants deficient in SOD and DNA repair genes $(sod^-\;xth^-\;and\;nfo^-)$ was demonstrated by transforming the mutant strain with a plasmid pYK9 which encoded Photobacterium leiognathi CuZnSOD and human AP endonuclease. The results show that survival rates were increased in $sod^+\;xth^-\;nfo^+$ cells compared to $sod^-\;xth^-\;ap^+,\;sod^-\;xth^-\;ap^-,\;and\;sod^+\;xth^-\;ap^-$ cells under oxidative stress generated from 0.1 mM Paraquat or 3 mM $H_2O_2$. The data suggested that, at least, SOD and DNA repair enzymes may have collaborate protection and repair of the damaged DNA. Additionally, both enzymes are required for protection against free radicals.

O-GlcNAcylation of p53 has been already identified and reported, but the function of O-GlcNAc on p53 has not been studied well. In this report, the general function of O-GlcNAc modification on p53 has been investigated using mouse fibroblast cell, L929. When streptozotocin (STZ), a non-competitive O-GlcNAcase inhibitor was treated to L929, O-GlcNAc modification level was dramatically increased on nucleocytoplasmic proteins, including p53. Because it has been already reported that $TNF\alpha$ induced the production of p53 in L929, $TNF\alpha$ was treated to obtain more p53. Approximately two times more amount of p53 was found from the cells treated STZ and $TNF\alpha$ simultaneously compared to the cell treated $TNF\alpha$ alone. The p53 increment in the presence of STZ was not caused by the induction of p53 gene expression. When new production of p53 induced by the $TNF\alpha$ was inhibited by the treatment of cycloheximide, O-GlcNAc modification decreased and phosphorylation increased on pre-existing p53 after $TNF\alpha$ treatment. But in the presence of STZ and $TNF\alpha$ at the same time, more O-GlcNAcylation occurred on p53, The level of ubiquitination on p53 was also reduced in the presence of STZ. Approximately three times less amount of Mdm2 bound to this hyperglycosylated p53. From this result it might be concluded that treatment of STZ to inhibit O-GlcNAcase increased O-GlcNAc modification level on p53 and the increment of O-GlcNAc modification stabilized p53 from ubiquitin proteolysis system.

Among biological hydrogen production processes, fermentative processes have some advantages. In this research, the hydrogen producing bacterium was isolated from domestic landfill area and identified as Enterobacter sp. The strain was named Enterobacter sp. SNU-1453. Important parameters for the hydrogen process include pH, temperature, concentration of initial glucose, and kind of sugars. The pH of the culture medium significantly decreased as fermentation proceeded due to the accumulation of various organic acids, and this inhibited the $H_2$ production seriously. When pH was controlled at pH 7.0, hydrogen production was 2614.5 m1/1 in 17 hours. The increase of glucose concentration resulted in higher $H_2$ production. The productivity of this strain was 6.87 mmol $H_2/l$ per hi on concentration of 25g glucose/l. Enterobacter sp. SNU-1453 could utilize various sugars. These results indicate that Enterobacter sp. SNU-1453 has a high potential as a fermentative $H_2$ producer.

Understanding the molecular pathogenesis of the multifaceted host-pathogen interaction is critical in the development of improved treatment and prevention, as well as elucidating how certain bacteria can circumvent host defenses, multiply in the host, and cause such extensive damage. Disease caused by infection with V. vulnificus is remarkable for the invasive nature of the infection, ensuing severe tissue damage, and rapidly fulminating course. The characterization of somatic as well as secreted products of V. vulnificus has yielded a large list of putative virulence attributes, whose known functions are easily imagined to explain the pathology of disease. These putative virulence factors include a carbohydrate capsule, lipopolysaccharide, a cytolysin/hemolysin, elastolytic metalloprotease, iron sequestering systems, lipase, and pili. However, only few among the putative virulence factors has been confirmed to be essential for virulence by the use of molecular Koch's postulates. This presentation describes molecular biological characterization of the virulence factors contributing to survival as well as to toxigenesis of V. vulnificus.

SPIN90 was identified to farm molecular complex with $\betaPIX$, WASP and Nck. This complex shows that SPIN90 interacts with Nck in a manner dependent upon cell adhesion to extracellular matrix, but $SPIN90{\cdot}{\beta}PIX{\cdot}WASP$ complex was stable even in suspended cells. This suggests that SPIN90 serves as an adaptor molecule to recruit other proteins to Nck at focal adhesions. SPIN90 was phosphorylated by ERK1, which was, itself, activated by cell adhesion and platelet-derived growth factor. Such phosphorylation of SPIN90 likely promotes the interaction of the $SPIN90{\cdot}{\beta}PIX{\cdot}WASP$ complex and Nck. It thus appears that the interaction of the $SPIN90{\cdot}{\beta}PIX{\cdot}WASP$ complex with Nck is crucial for stable cell adhesion and can be dynamically modulated by SPIN90 phosphorylation that is dependent on cell adhesion and ERX activation. SPIN90 directly binds syndapin I, syndapin isoform II-1 and II-s via its PRD region in vitro, in vivo and also associates with endocytosis core components such as clathrin and dynamin. In neuron and fibroblast, SPIN90 colocalizes with syndapins as puntate form, consistent with a role for SPIN90 in clathrin-mediated endocytosis pathway. Overexpression of SPIN90 N-term inhibits receptor-mediated endocytosis. Interestingly, SPIN90 PRD, binding interface of syndapin, significantly blocks internalization of transferrin, demonstrating SPIN90 involvement in endocytosis in vivo by interacting syndapin. Depletion of endogenous SPIN90 by introducing $\alpha-SPIN90$ also blocks receptor-mediated endocytosis. Actin polymerization could generate farce facilitating the pinch-out event in endocytosis, detach newly formed endocytic vesicle from the plasma membrane or push out them via the cytosol on actin tails. Here we found that SPIN90 localizes to high actin turn over cortical area, actin-membrane interface and membrane ruffle in PDGF treated cells. Overexpression of SPIN90 has an effect on cortical actin rearrangement as filopodia induction and it is mediated by the Arp2/3 complex at cell periphery. Consistent with a role in actin organization, CFP-SPIN90 present in actin comet tail generated by PIP5 $kinase\gamma$ overexpression. Therefore this study suggests that SPIN90 is functional linker between endocytosis and actin cytoskeleton.