BETA-AMINOBUTYRIC ACID INDUCES THE ACCUMULATION OF PATHOGENESIS-RELATED PROTEINS IN TOMATO (LYCOPERSICON-ESCULENTUM L.) PLANTS AND RESISTANCE TO LATE BLIGHT INFECTION CAUSED BY PHYTOPHTHORA-INFESTANS

Citation
Y. Cohen et al., BETA-AMINOBUTYRIC ACID INDUCES THE ACCUMULATION OF PATHOGENESIS-RELATED PROTEINS IN TOMATO (LYCOPERSICON-ESCULENTUM L.) PLANTS AND RESISTANCE TO LATE BLIGHT INFECTION CAUSED BY PHYTOPHTHORA-INFESTANS, Plant physiology, 104(1), 1994, pp. 59-66
Citations number
33
Categorie Soggetti
Plant Sciences
Journal title
ISSN journal
00320889
Volume
104
Issue
1
Year of publication
1994
Pages
59 - 66
Database
ISI
SICI code
0032-0889(1994)104:1<59:BAITAO>2.0.ZU;2-P
Abstract
Tomato (Lycopersicon esculentum L.) plants were sprayed with aqueous s olutions of isomers of aminobutyric acid and were either analyzed for the accumulation of pathogenesis-related (PR) proteins or challenged w ith the late blight fungal agent Phytophthora infestans. The beta isom er of aminobutyric acid induced the accumulation of high levels of thr ee proteins: P14a, beta-1,3 glucanase, and chitinase. These proteins e ither did not accumulate or accumulated to a much lower level in alpha - or gamma-aminobutyric acid-treated plants. Plants pretreated with al pha-, beta-, and gamma-aminobutyric acid were protected up to 11 d to an extent of 35, 92, and 6%, respectively, against a challenge infecti on with P. infestans. Protection by beta-aminobutyric acid was afforde d against the blight even when the chemical was applied 1. d postinocu lation. Examination of ethylene evolution showed that alpha-aminobutyr ic acid induced the production of 3-fold higher levels of ethylene com pared with beta-aminobutyric acid, whereas gamma-aminobutyric acid ind uced no ethylene production. In addition, silver thiosulfate, a potent inhibitor of ethylene action, did not abolish the resistance induced by beta-aminobutyric acid. The results are consistent with the possibi lity that beta-aminobutyric acid protects tomato foliage against the l ate blight disease by a mechanism that is not mediated by ethylene and that PR proteins can be involved in induced resistance.