Movement of plant viruses is delayed in a beta-1,3-glucanase-deficient mutant showing a reduced plasmodesmatal size exclusion limit and enhanced callose deposition

Susceptibility to virus infection is decreased in a class I beta-1,3-glucan ase (GLU I)-deficient mutant (TAG4.4) of tobacco generated by antisense tra nsformation. TAG4.4 exhibited delayed intercellular trafficking via plasmod esmata of a tobamovirus (tobacco mosaic virus), of a potexvirus (recombinan t potato virus X expressing GFP), and of the movement protein (MP) 3a of a cucumovirus (cucumber mosaic virus). Monitoring the cell-to-cell movement o f dextrans and peptides by a novel biolistic method revealed that the plasm odesmatal size exclusion limit (SEL) of TAG4.4 was also reduced from 1.0 to 0.85 nm. Therefore, GLU I-deficiency has a broad effect on plasmodesmatal movement, which is not limited to a particular virus type. Deposition of ca llose, a substrate for beta-1,3-glucanases, was increased in TAG4.4 in resp onse to 32 degrees C treatment, treatment with the fungal elicitor xylanase , and wounding, suggesting that GLU I has an important function in regulati ng callose metabolism. Callose turnover is thought to regulate plasmodesmat al SEL. We propose that GLU I induction in response to infection may help p romote MP-driven virus spread by degrading callose.