BackgroundSwitchgrass is one of the most promising bioenergy crop candidates for the US. It gives relatively high biomass yield and can grow on marginal lands. However, its yields vary from year to year and from location to location. Thus it is imperative to develop a low input and sustainable switchgrass feedstock production system. One of the most feasible ways to increase biomass yields is to harness benefits of microbial endophytes.ResultsWe demonstrate that one of the most studied plant growth promoting bacterial endophytes, Burkholderia phytofirmans strain PsJN, is able to colonize and significantly promote growth of switchgrass cv. Alamo under in vitro, growth chamber, and greenhouse conditions. In several in vitro experiments, the average fresh weight of PsJN-inoculated plants was approximately 50% higher than non-inoculated plants. When one-month-old seedlings were grown in a growth chamber for 30 days, the PsJN-inoculated Alamo plants had significantly higher shoot and root biomass compared to controls. Biomass yield (dry weight) averaged from five experiments was 54.1% higher in the inoculated treatment compared to non-inoculated control. Similar results were obtained in greenhouse experiments with transplants grown in 4-gallon pots for two months. The inoculated plants exhibited more early tillers and persistent growth vigor with 48.6% higher biomass than controls. We also found that PsJN could significantly promote growth of switchgrass cv. Alamo under sub-optimal conditions. However, PsJN-mediated growth promotion in switchgrass is genotype specific.ConclusionsOur results show B. phytofirmans strain PsJN significantly promotes growth of switchgrass cv. Alamo under different conditions, especially in the early growth stages leading to enhanced production of tillers. This phenomenon may benefit switchgrass establishment in the first year. Moreover, PsJN significantly stimulated growth of switchgrass cv. Alamo under sub-optimal conditions, indicating that the use of the beneficial bacterial endophytes may boost switchgrass growth on marginal lands and significantly contribute to the development of a low input and sustainable feedstock production system.

Yokota suggested an optimistic limit method of the Kashaev invariants of hyperbolic knots and showed it determines the complex volumes of the knots. His method is very effective and gives almost combinatorial method of calculating the complex volumes. However, to describe the triangulation of the knot complement, he restricted his method to knot diagrams with certain conditions. Although these restrictions are general enough for any hyperbolic knots, we have to select a good diagram of the knot to apply his theory.In this article, we suggest more combinatorial way to calculate the complex volumes of hyperbolic links using the modified optimistic limit method. This new method works for any link diagrams, and it is more intuitive, easy to handle and has natural geometric meaning.

It is known that a knot complement can be decomposed into ideal octahedra along a knot diagram. A solution to the gluing equations applied to this decomposition gives a pseudo-developing map of the knot complement, which will be called a pseudo-hyperbolic structure. In this paper, we study these in terms of segment and region variables which are motivated by the volume conjecture so that we can compute complex volumes of all the boundary parabolic representations explicitly. We investigate the octahedral developing and holonomy representation carefully, and obtain a concrete formula of Wirtinger generators for the representation and also of cusp shape. We demonstrate explicit solutions for T (2, N ) torus knots, J(N, M ) knots and also for other interesting knots as examples. Using these solutions we can observe the asymptotic behavior of complex volumes and cusp shapes of these knots. We note that this construction works for any knot or link, and reflects systematically both geometric properties of the knot complement and combinatorial aspects of the knot diagram.

An analysis of the interannual variability of surface air temperature during the boreal winter in the East Asian (EA) region from 1960 to 2009 reveals that the East Asian winter monsoon (EAWM) significantly weakens after the mid-1980s. The robust warming over the EA region in the lower and middle troposphere as well as at the surface is caused mainly by changes in circulations over the North Pacific and Eurasian continent. The 300 hPa East Asian jet and 500 hPa trough over the EA region, which are closely linked to cold surges, significantly weaken after the mid-1980s. The weakened northerly wind in the Siberian high region and north of the EA region interfere with cold advection toward the EA region. The anomalous southeasterlies over the East China Sea due to an enhanced North Pacific oscillation (NPO)-like sea level pressure (SLP) pattern lead to anomalous warm advection over the EA region. It is also found that the advection of mean temperature by anomalous wind and the advection of anomalous temperature by mean wind mainly contribute to the anomalous warm advection in the EA region after the mid-1980s. Consequently, these anomalous circulations provide a more favorable environment for weakening of the EAWM.

BackgroundMycobacterium smegmatis, a rapidly growing non-tuberculosis mycobacterium, is a good model for studying the pathogenesis of tuberculosis because of its genetic similarity to Mycobacterium tuberculosis (Mtb). Macrophages remove mycobacteria during an infection. Macrophage apoptosis is a host defense mechanism against intracellular bacteria. We have reported that endoplasmic reticulum (ER) stress is an important host defense mechanism against Mtb infection.ResultsIn this study, we found that M. smegmatis induced strong ER stress. M. smegmatis-induced reactive oxygen species (ROS) play a critical role in the induction of ER stress-mediated apoptosis. Pretreatment with an ROS scavenger suppressed M. smegmatis-induced ER stress. Elimination of ROS decreased the ER stress response and significantly increased the intracellular survival of M. smegmatis. Interestingly, inhibition of phagocytosis significantly decreased ROS synthesis, ER stress response induction, and cytokine production.ConclusionsPhagocytosis of M. smegmatis induces ROS production, leading to production of proinflammatory cytokines. Phagocytosis-induced ROS is associated with the M. smegmatis-mediated ER stress response in macrophages. Therefore, phagocytosis plays a critical role in the induction of ER stress-mediated apoptosis during mycobacterial infection.

No abstract

Mycobacterium fortuitum (MF), a rapidly growing nontuberculosis mycobacterium, is recognized as an important human pathogen. We investigated whether the endoplasmic reticulum (ER) stress response is associated with the apoptosis of MF-infected macrophages. The expression of ER molecular chaperones was significantly induced by MF infection. We found that MF-induced reactive oxygen species (ROS) generation plays a critical role in the induction of ER stress-mediated apoptosis. Excess TNF-α in the ER led to ER stress-mediated apoptosis during MF infection. The intracellular survival of MF was significantly increased by TNF-α knockdown compared with the control. This is the first report of MF-induced TNF-α as a cause of ER stress in macrophages. Furthermore, we found that TLR2-mediated ER stress response contributed to the elimination of intracellular MF in vivo. These results suggest that TNF-α-mediated ER stress during MF infection contributes to the suppression of intracellular survival of MF in macrophages. Our findings provide new insight into the importance of ER stress in mycobacterial infection.-Oh, S.-M., Lim, Y.-J., Choi, J.-A., Lee, J., Cho, S.-N., Go, D., Kim, S.-H., Song, C.-H. TNF-α-mediated ER stress causes elimination of Mycobacterium fortuitum reservoirs by macrophage apoptosis.

Endoplasmic reticulum (ER)-stress-mediated apoptosis is a host defense mechanism against Mycobacterium tuberculosis (Mtb) infection. Calreticulin (CRT) is the major calcium-binding chaperone protein. Previous reports have suggested a close relationship between the cell-surface expression of CRT and apoptosis. In this study, the role of CRT during Mtb infection was examined. The results showed that Mtb infection induces CRT production by macrophages and that CRT levels are correlated with the degree of apoptotic cell death. The enhanced production of CRT was associated with the ER stress induced by Mtb infection. A significant increase in CRT translocation from the cytosol to the plasma membrane after 24 h of infection suggested the importance of CRT localization in the induction of apoptosis during Mtb infection. An investigation of the factors associated with CRT translocation and the ability of ectopically expressed CRT to induce apoptosis showed that pretreatment with a reactive oxygen species scavenger decreased Mtb-induced CRT expression, leading to the reduction of CHOP and caspase-3 activation. The intracellular survival of Mtb was significantly higher in macrophages transfected with a CRT-specific small interfering RNA than in control cells. The key role of CRT in inducing apoptosis included its interaction with CXCR1 and TNFR1 in Mtb-infected macrophages. The CRT/CXCR1/TNFR1 complex was shown to induce the extrinsic apoptotic pathway during Mtb infection. Together, these results demonstrate that CRT is critical for the intracellular survival of Mtb, via ER-stress-induced apoptosis, as well as the importance of ER stress-mediated CRT localization in the pathogenesis of tuberculosis.