Regulation of carbohydrate partitioning during the interaction of potato virus Y with tobacco

被引:116
作者
Herbers, K. [1 ]
Takahata, Y. [1 ]
Melzer, M. [1 ]
Mock, H. -P. [1 ]
Hajirezaei, M. [1 ]
Sonnewald, U. [1 ]
机构
[1] Inst Pflanzengenet & Kulturpflanzenforsch, D-06466 Gatersleben, Germany
关键词
D O I
10.1046/j.1364-3703.2000.00007.x
中图分类号
Q94 [植物学];
学科分类号
071001 ;
摘要
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.
引用
收藏
页码:51 / 59
页数:9
相关论文
共 44 条
[1]  
[Anonymous], 1996, PHOTOASSIMILATE DIST
[2]   Concepts of plant biotic stress. Some insights into the stress physiology of virus-infected plants, from the perspective of photosynthesis [J].
Balachandran, S ;
Hurry, VM ;
Kelley, SE ;
Osmond, CB ;
Robinson, SA ;
Rohozinski, J ;
Seaton, GGR ;
Sims, DA .
PHYSIOLOGIA PLANTARUM, 1997, 100 (02) :203-213
[3]   ARABIDOPSIS MUTANTS SIMULATING DISEASE RESISTANCE RESPONSE [J].
DIETRICH, RA ;
DELANEY, TP ;
UKNES, SJ ;
WARD, ER ;
RYALS, JA ;
DANGL, JL .
CELL, 1994, 77 (04) :565-577
[4]   Photosynthetic properties of leaves of Eupatorium makinoi infected by a geminivirus [J].
Funayama, S ;
Sonoike, K ;
Terashima, I .
PHOTOSYNTHESIS RESEARCH, 1997, 53 (2-3) :253-261
[5]   REQUIREMENT OF SALICYLIC-ACID FOR THE INDUCTION OF SYSTEMIC ACQUIRED-RESISTANCE [J].
GAFFNEY, T ;
FRIEDRICH, L ;
VERNOOIJ, B ;
NEGROTTO, D ;
NYE, G ;
UKNES, S ;
WARD, E ;
KESSMANN, H ;
RYALS, J .
SCIENCE, 1993, 261 (5122) :754-756
[6]   REGULATION OF PHOTOSYNTHESIS BY END-PRODUCT ACCUMULATION IN LEAVES OF PLANTS STORING STARCH, SUCROSE, AND HEXOSE SUGARS [J].
GOLDSCHMIDT, EE ;
HUBER, SC .
PLANT PHYSIOLOGY, 1992, 99 (04) :1443-1448
[7]   PROGRAMMED CELL-DEATH IN PLANTS - A PATHOGEN-TRIGGERED RESPONSE ACTIVATED COORDINATELY WITH MULTIPLE DEFENSE FUNCTIONS [J].
GREENBERG, JT ;
GUO, AL ;
KLESSIG, DF ;
AUSUBEL, FM .
CELL, 1994, 77 (04) :551-563
[8]   Cloning of a tobacco apoplasmic invertase inhibitor - Proof of function of the recombinant protein and expression analysis during plant development [J].
Greiner, S ;
Krausgrill, S ;
Rausch, T .
PLANT PHYSIOLOGY, 1998, 116 (02) :733-742
[9]   Ectopic expression of a tobacco invertase inhibitor homolog prevents cold-induced sweetening of potato tubers [J].
Greiner, S ;
Rausch, T ;
Sonnewald, U ;
Herbers, K .
NATURE BIOTECHNOLOGY, 1999, 17 (07) :708-711
[10]   Molecular determinants of sink strength [J].
Herbers, K ;
Sonnewald, U .
CURRENT OPINION IN PLANT BIOLOGY, 1998, 1 (03) :207-216