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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]