β-1,3-Glucanase and the spread of tobacco mosaic virus in Nicotiana and Phaseolus

Abstract

The β-1,3-glucan callose is thought to form a seal which surrounds viral local lesions and prevents viral spread in many plant hosts. Therefore, we investigated the role of host β-1,3-glucanase in facilitating viral spread. The following were compared for lesion size (indicating viral spread rate) and β-1,3-glucanase activity: (i) inoculated excised leaves of Phaseolus vulgaris L. cv. Pinto supplied with sugar (small lesions) or deprived of sugar (large lesions); (ii) Nicotiana glutinosa L. infected with the VM strain (small lesions) or the U1 strain (large lesions) of tobacco mosaic virus; and (iii) Nicotiana sylvestris Spegaz. infected with the VM strain (small lesions) or the U2 strain (large lesions) of tobacco mosaic virus. In all cases, the larger, more rapidly spreading viral lesions did not have significantly higher levels of β-1,3-glucanase activity than the corresponding smaller lesions. Nicotiana sylvestris leaves with a systemic viral infection had a β-1,3-glucanase activity lower than that of leaves with local lesions. Finally, β-1,3-glucanase activity was stimulated to the same extent by a slowly developing abiotic necrosis as by local lesions of tobacco mosaic virus, β-1,3-Glucanase activity may therefore increase during localized viral infection as a result of the wounding associated with necrotic viral lesions.