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

Abstract

SummaryMutant tobacco plants de®cient for class I b-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 b-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 ®rst direct evidence that a biological function of a plant b-1,3-glucanase depends on its catalytic activity.

Induction of systemic resistance against tobacco mosaic virus by Ningnanmycin in tobacco

“…Many studies have confirmed that the b-1,3-glucanases play a role in mechanism involved in resistance to pathogenic infection, which are coordinately induced in response to pathogenic infection and it can be considered as pathogenesis-related protein of tobacco [28][29][30][31][32]. Our results demonstrated that that the activity of b-1,3-glucanases obviously increased in the presence of NNM (Fig.…”

Tobacco mosaic virus infection spreads cell to cell as intact replication complexes

“…As described above, a period of 1-2 h is required for passage of VMCs; this need may indicate that biochemical changes, which cause temporary changes in size exclusion limits of the plasmodesmata (48), take place during this period. Other workers have shown that ␤-1,3 glucanase plays a role in controlling cell-cell spread of infection by TMV (49,50). We propose that activity of this enzyme and͞or other host proteins during the period that VRCs are tightly appressed to plasmodesmata, are important, if not essential, for cell-cell spread of the VMCs.…”

ArabidopsisPumilio protein APUM5 suppressesCucumber mosaic virusinfection via direct binding of viral RNAs

“…These processes occur upon the interaction between the virus and host proteins or after the suppression of the host basal defense mechanism and often lead to abnormal phenotypes of virus-infected host plants, such as small, highly branched bushes with deformed leaves, stunting, and reduced apical dominance (2)(3)(4). Thus, the reduced growth and developmental changes in the virus-infected plants are typical symptoms of virus infection and signify that the virus has undergone a successful life cycle.…”