Summary Myo‐inositol‐1‐phosphate synthase (MIPS) is a key rate limiting enzyme in myo‐inositol biosynthesis. The MIPS gene has been shown to improve tolerance to abiotic stresses in several plant species. However, its role in resistance to biotic stresses has not been reported. In this study, we found that expression of the sweet potato IbMIPS1 gene was induced by NaCl, polyethylene glycol (PEG), abscisic acid (ABA) and stem nematodes. Its overexpression significantly enhanced stem nematode resistance as well as salt and drought tolerance in transgenic sweet potato under field conditions. Transcriptome and real‐time quantitative PCR analyses showed that overexpression of IbMIPS1 up‐regulated the genes involved in inositol biosynthesis, phosphatidylinositol (PI) and ABA signalling pathways, stress responses, photosynthesis and ROS‐scavenging system under salt, drought and stem nematode stresses. Inositol, inositol‐1,4,5‐trisphosphate (IP3), phosphatidic acid (PA), Ca2+, ABA, K+, proline and trehalose content was significantly increased, whereas malonaldehyde (MDA), Na+ and H2O2 content was significantly decreased in the transgenic plants under salt and drought stresses. After stem nematode infection, the significant increase of inositol, IP3, PA, Ca2+, ABA, callose and lignin content and significant reduction of MDA content were found, and a rapid increase of H2O2 levels was observed, peaked at 1 to 2 days and thereafter declined in the transgenic plants. This study indicates that the IbMIPS1 gene has the potential to be used to improve the resistance to biotic and abiotic stresses in plants.

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Staphylococcus aureus is an important human pathogen that is the principal cause of a variety of diseases, ranging from localized skin infections to life-threatening systemic infections. The success of the organism as a pathogen and its ability to cause such a wide range of infections are due to its extensive virulence factors. In this study, we identified the role of the only GGDEF domain protein (GdpS [GGDEF domain protein from Staphylococcus]) in the virulence of S. aureus NCTC8325. Inactivation of gdpS results in an alteration in the production of a range of virulence factors, such as serine and cysteine proteases, fibrinogen-binding proteins, and, specifically, protein A (Spa), a major surface protein of S. aureus. The transcript level of spa decreases eightfold in the gdpS mutant compared with the parental NCTC8325 strain. Furthermore, the transcript level of sarS, which encodes a direct positive regulator of spa, also decreases in the gdpS mutant compared with the wild type, while the transcript levels of agr, sarA, sarT, and rot display no apparent changes in the gdpS mutant, suggesting that GdpS affects the expression of spa through interaction with SarS by unknown mechanisms. Furthermore, the complementation assays show that the influences of GdpS on spa and sarS depend on its N-terminal domain, which is predicted to be the sensor of a two-component system, rather than its C-terminal GGDEF domain with conserved GGDEF, suggesting that GdpS functions in S. aureus by an unknown mechanism independent of 3,5-cyclic diguanylic acid signaling.Staphylococcus aureus is a well-known human pathogen which is the most common cause of a broad range of infections in humans involving all organ systems, ranging from localized skin infections to life-threatening systemic infections (3, 30). Production of a wide range of virulence factors is thought to be a key to this organism's ability to colonize, infect, and eventually cause disease in its host tissue (4, 27). These factors include secreted proteins, such as serine and cysteine proteases, nuclease, hemolysins, enterotoxins, lipase, and coagulase, and proteins exposed on the cell surface, such as protein A (Spa) and fibrinogen-, fibronectin-, and collagen-binding proteins (14,34). Most of the studies of the mechanisms of staphylococcal pathogenesis have focused mainly on the regulatory mechanisms involved in the virulence factor gene expression in order to institute a more efficient infection control model (4,10,33).Among the many virulence factors, Spa is a cell wall-associated exoprotein that binds to the Fc regions of immunoglobulin Gs (IgG) of diverse mammalian species and is thought to be an important component of the immune evasion machinery of this pathogen (16,21,29,45). Previous studies have shown that strains of S. aureus with a high Spa content are more resistant to phagocytosis by human neutrophils in vitro than strains with smaller amount of Spa, possibly owing to the IgG Fc-binding property of Spa. The role of Spa in the pathogenesis of staphylococcal in...

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