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

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Abstract
Summary: Susceptibility to virus infection is decreased in a class I β‐1,3‐glucanase (GLU I)‐deficient mutant (TAG4.4) of tobacco generated by antisense transformation. TAG4.4 exhibited delayed intercellular trafficking via plasmodesmata of a tobamovirus (tobacco mosaic virus), of a potexvirus (recombinant potato virus X expressing GFP), and of the movement protein (MP) 3a of a cucumovirus (cucumber mosaic virus). Monitoring the cell‐to‐cell movement of dextrans and peptides by a novel biolistic method revealed that the plasmodesmatal 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 callose, a substrate for β‐1,3‐glucanases, was increased in TAG4.4 in response to 32°C treatment, treatment with the fungal elicitor xylanase, and wounding, suggesting that GLU I has an important function in regulating callose metabolism. Callose turnover is thought to regulate plasmodesmatal SEL. We propose that GLU I induction in response to infection may help promote MP‐driven virus spread by degrading callose.