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

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Mutant tobacco plants deficient for class I β-1,3-glucanase (GLU I) are decreased in their susceptibility to virus infection. This is correlated with delayed virus spread, a reduction in the size exclusion limit of plasmodesmata and increased cell-wall deposition of the β-1,3-glucan callose. To further investigate a role of GLU I during cell-to-cell movement of virus infection, we inserted the GLU I coding sequence into TMV for overexpression 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. Viruses expressing antisense GLU I constructs led to lesions of decreased size. Similar effects were obtained for virus spread using plants grown at 32°C to block the hypersensitive response. Together, these results indicate that enzymatically active GLU I expressed in cells containing replicating virus can increase cell-to-cell movement of virus. This supports the view that GLU I induced locally during infection helps to promote cell-to-cell movement of virus by hydrolyzing callose. Moreover, our results provide the first direct evidence that a biological function of a plant β-1,3-glucanase depends on its catalytic activity.
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Keywords: 3-glucanase; TMV; callose; plasmodesmata; tobacco; virus spread; β-1

Document Type: Research Article

Affiliations: Friedrich Miescher Institute, A Branch of the Novartis Research Foundation, Maulbeerstrasse 66, CH-4058 Basel, Switzerland

Publication date: November 1, 2001

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