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Wound‐induced PAL activity is suppressed by heat‐shock treatments that induce the synthesis of heat‐shock proteins
Author(s) -
Kang HoMin,
Saltveit Mikal E.
Publication year - 2003
Publication title -
physiologia plantarum
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.351
H-Index - 146
eISSN - 1399-3054
pISSN - 0031-9317
DOI - 10.1034/j.1399-3054.2003.00190.x
Subject(s) - heat shock protein , browning , heat shock , biochemistry , shock (circulatory) , hsp60 , phenylalanine ammonia lyase , chemistry , protein biosynthesis , western blot , microbiology and biotechnology , phenylalanine , biology , hsp70 , amino acid , medicine , gene
Wounding lettuce leaves induces the de novo synthesis of phenylalanine ammonia‐lyase (PAL, EC 4.3.1.5), the accumulation of phenolic compounds, and subsequent tissue browning. A brief heat‐shock at 45°C reduces the rise in wound‐induced PAL, the accumulation of phenolic compounds, and tissue browning. The activity of PAL measured 24 h after wounding and the content of phenolic compounds (absorbance of methanol extract at 320 nm) measured 48 h after wounding was highly correlated (R 2 > 0.90) in tissue developing the normal wound response and in tissue subjected to 0–180 s of heat‐shock after wounding. The synthesis of a unique set of proteins called heat‐shock proteins (hsps) is induced by these heat‐shock treatments. Western‐blot analyses of proteins isolated from wounded and heat‐shocked Iceberg and Romaine lettuce mid‐rib leaf tissue was done using antibodies against hsp 23. Only those heat‐shock treatments that were effective at inducing the synthesis of hsp 23 were effective in reducing the activity of PAL induced by wounding and the subsequent accumulation of phenolic compounds. Hsps induced in non‐wounded, whole leaves by exposure to 45°C for 150 s did not significantly interact with PAL previously synthesized in non‐heat‐shocked wounded leaves to limit its activity. The preferential synthesis of hsps over that of wound‐induced PAL, rather than the presence of hsps, may be responsible for the ability of a heat‐shock treatment to reduce the wound‐induced increase in PAL activity. Our results support this novel concept, and the possibility that heat‐shock treatments can have significant physiological effects on the response of the tissue to other stresses, not because of the specific genes they induce or repress, or the products they cause to be synthesized, but by their secondary action of influencing the synthesis of other proteins (e.g. PAL) by the suppression of non‐hsps protein synthesis.