Abstract:
:Abstract To test whether carbohydrates may play a signalling function during plant pathogenesis, we investigated the interaction between tobacco and potato virus Y (PVY(N)). Four days after PVY(N) infection, leaves started to accumulate soluble sugars and leaf photosynthesis decreased. The accumulation of soluble sugars was accompanied by an induction of cell wall invertase and a gradual decrease in the sucrose-to-hexose ratio. In parallel to changes in carbohydrate metabolism and photosynthesis, transcripts encoding PR-proteins accumulated. Based on this coincidence, it was hypothesized that elevated hexose levels may enhance the expression of defence-related functions and might possibly explain the phenomenon of high sugar resistance in plants. This notion has been supported by the fact that cell wall invertase-expressing transgenic tobacco plants were found to be resistant against PVY(N) (Herbers et al., 1996b). To exclude the possibility that salicylate, which accumulates in plants expressing invertase, may be responsible for the observed resistance, these transgenic plants were crossed with salicylate hydroxylase-expressing plants (nahG). The progeny were selected for high levels of sugar and low levels of salicylate. Necrotic lesions also developed, typically formed on the leaves of plants expressing invertase, and transcripts encoding PR-Q accumulated in the absence of salicylate. On the other hand, accumulation of PR-1b transcripts decreased, indicating that sugars are not sufficient for PR-1b induction. Infection experiments using these plants as hosts revealed resistance towards PVY(N). Thus, the mechanism of apoplastic invertase induced virus resistance is salicylate independent and most likely sugar mediated.
journal_name
Mol Plant Patholjournal_title
Molecular plant pathologyauthors
Herbers K,Takahata Y,Melzer M,Mock HP,Hajirezaei M,Sonnewald Udoi
10.1046/j.1364-3703.2000.00007.xsubject
Has Abstractpub_date
2000-01-01 00:00:00pages
51-9issue
1eissn
1464-6722issn
1364-3703pii
MPP007journal_volume
1pub_type
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