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Microtubules, one of the cytoskeletons, are highly dynamic structures that play a variety of roles in maintaining cell morphology, cell division and intracellular transport. Microtubules are composed of heterodimers of α- and β-tubulins, which are repeatedly polymerized and depolymerized. To investigate the radiation-induced impacts on the polymerization reaction of tubulins, we evaluated the molecular interactions between normal and irradiated tubulins. First, the polymerization reaction of the tubulins was measured after stepwise irradiation from 0 Gy to 1,000 Gy of X rays. The polymerization was inhibited in a dose-dependent manner. Next, the tubulins' polymerization reaction was then measured after the tubulin that was damaged from the exposure to 1,000 Gy of X rays was mixed with the normal tubulins. Our findings reveal that the radiation dose-dependent change in the degree of overall microtubule polymerization progression depends on the ratio of damaged tubulin. This result is biochemical evidence that non-DNA damage (in this case, cytoskeletal damage) from cytoplasmic radiation exposure may inhibit cell division, suggesting that some cytoskeletal damage may also affect the fate of the entire cell. [ABSTRACT FROM AUTHOR]

The cystine/glutamate antiporter, system xc−, is essential for the efficient uptake of cystine into cells. Interest in the mechanisms of system xc− function soared with the recognition that system xc− presents the most upstream node of ferroptosis, a recently described form of regulated necrosis relevant for degenerative diseases and cancer. Since targeting system xc− hold the great potential to efficiently combat tumor growth and metastasis of certain tumors, we disrupted the substrate‐specific subunit of system xc−, xCT (SLC7A11) in the highly metastatic mouse B16F10 melanoma cell line and assessed the impact on tumor growth and metastasis. Subcutaneous injection of tumor cells into the syngeneic B16F10 mouse melanoma model uncovered a marked decrease in the tumor‐forming ability and growth of KO cells compared to control cell lines. Strikingly, the metastatic potential of KO cells was markedly reduced as shown in several in vivo models of experimental and spontaneous metastasis. Accordingly, survival rates of KO tumor‐bearing mice were significantly prolonged in contrast to those transplanted with control cells. Analyzing the in vitro ability of KO and control B16F10 cells in terms of endothelial cell adhesion and spheroid formation revealed that xCT expression indeed plays an important role during metastasis. Hence, system xc− emerges to be essential for tumor metastasis in mice, thus qualifying as a highly attractive anticancer drug target, particularly in light of its dispensable role for normal life in mice. What's new? The cystine/glutamate antiporter system xc‐ has generated growing interest as the most upstream node of ferroptosis, a recently‐described iron‐dependent form of necrotic cell death that is highly relevant in cancer. Using mouse cell‐based assays and in vivo murine cancer models, here the authors demonstrate that system xc‐deficiency not only impairs primary tumor growth but also abrogates tumor dissemination and metastasis in melanoma. The results also show in tumor‐bearing mice that reduced metastasis coincides with increased overall survival. Overall, the findings support the essential role of system xc‐ in tumor metastasis and its potential as an attractive anti‐cancer drug target. [ABSTRACT FROM AUTHOR]

To identify apoplasmic proteins in grape cells, we investigated proteins secreted into grape cell culture medium and detected β-1,3-glucanase VvGHF17 in the medium. VvGHF17 is expressed constitutively in grape leaves and berry pulp and skin. Experiments using VvGHF17:GFP fusion protein demonstrated that VvGHF17 is localized at the apoplasmic space of cells, suggesting that VvGHF17 is apoplasmic β-1,3-glucanase. To understand how VvGHF17 protects grapevine against phytopathogens, we created Arabidopsis transgenic plants expressing VvGHF17. VvGHF17-expressing Arabidopsis plants exhibited disease resistance to both Botrytis cinerea and Colletotrichum higginsianum , but not to Pseudomonas syringae pv. tomato DC3000. The inhibitory effect of VvGHF17 to the infection by the fungi was promoted when VvGHF17 protein was expressed in large amounts in the plants. In conclusion, apoplasmic VvGHF17 may be a candidate for the transgene to create transgenic grapevines that are robust to multiple fungal attacks. [ABSTRACT FROM AUTHOR]

Abstract: It has been demonstrated that intestinal commensal bacteria induce immunoglobulin (Ig) A production by promoting the development of gut-associated lymphoid tissues in the small intestine. However, the precise mechanism whereby these bacteria modulate IgA production in the large intestine, which harbors the majority of intestinal commensals, is poorly understood. In addition, it is not known which commensal bacteria induce IgA production in the small intestine and which induce production in the large intestine. To address these issues, we generated gnotobiotic mice mono-associated with different murine commensal bacteria by inoculating germ-free (GF) mice with Lactobacillus johnsonii or Bacteroides acidifaciens. In GF mice, IgA production was barely detectable in the small intestine and was not detected in the large intestine. Interestingly, total IgA secretion in the large intestinal mucosa of B. acidifaciens mono-associated (BA) mice was significantly greater than that of GF and L. johnsonii mono-associated (LJ) mice. However, there was no difference in total IgA production in the small intestine of GF, LJ and BA mice. In addition, in the large intestine of BA mice, the expression of IgA+ cells and germinal center formation were more remarkable than in GF and LJ mice. Furthermore, B. acidifaciens-specific IgA was detected in the large intestine of BA mice. These results suggest that the production of IgA in the large intestine may be modulated by a different mechanism than that in the small intestine, and that B. acidifaciens is one of the predominant bacteria responsible for promoting IgA production in the large intestine. [Copyright &y& Elsevier]