Local expression of enzymatically active class I beta-1,3-glucanase enhances symptoms of TMV infection in tobacco

Mutant tobacco plants deficient for class I beta -1,3-glucanase (GLU I) are decreased in their susceptibility to virus infection. This is correlated w ith delayed virus spread, a reduction in the size exclusion limit of plasmo desmata and increased cell-wall deposition of the beta -1,3-glucan callose. To further investigate a role of GLU I during cell-to-cell movement of vir us infection, we inserted the GLU I coding sequence into TMV for overexpres sion in infected cells. Compared with the size of local lesions produced on plants infected with virus expressing either an enzymatically inactive GLU I or a frameshift mutant of the gene, the size of local lesions caused by infection with virus expressing active GLU I was consistently increased. Vi ruses expressing antisense GLU I constructs led to lesions of decreased siz e. Similar effects were obtained for virus spread using plants grown at 32 degreesC to block the hypersensitive response. Together, these results indi cate that enzymatically active GLU I expressed in cells containing replicat ing virus can increase cell-to-cell movement of virus. This supports the vi ew that GLU I induced locally during infection helps to promote cell-to-cel l movement of virus by hydrolyzing callose. Moreover, our results provide t he first direct evidence that a biological function of a plant beta -1,3-gl ucanase depends on its catalytic activity.