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In vivo evidence for the involvement of phospholipase A and protein kinase in the signal transduction pathway for auxin‐induced corn coleoptile elongation
Author(s) -
Yi Hanju,
Park Doonam,
Lee Youngsook
Publication year - 1996
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 - 10.1111/j.1399-3054.1996.tb00445.x
Subject(s) - coleoptile , auxin , signal transduction , microbiology and biotechnology , phospholipase c , elongation , phospholipase , in vivo , protein kinase a , chemistry , biology , biochemistry , kinase , enzyme , gene , materials science , ultimate tensile strength , metallurgy
Auxin‐induced elongation of com coleoptiles is accompanied by cell wall acidification, which depends upon H + ‐pump activity. We tested the hypothesis that phospholipase A and a protein kinase are involved in the pathway of auxin signal transduction leading to H + secretion, and elongation of corn coleoptiles. Initially, the pH of the bath solution at 50–100 μm from the surface of a coleoptile segment (pH o ) ranged between 4.8 and 6.6 when measured with an H + ‐sensitive microelectrode. Twenty or 50 μ M lysophosphatidylcholine, 50 μ M linolenic acid or 50 μ M arachidonic acid induced a decline in pH o by 0.3 to 2.1 units. The effect was blocked by 1 m M vanadate, suggesting that lysophosphatidylcholine or linolenic acid induced acidification of the apoplast by activating the H + ‐pump. Lysophosphatidylcholine and linolenic acid also accelerated the elongation rate of the coleoptiles. While linolenic acid and arachidonic acid, highly unsaturated fatty acids, promoted pH o decrease and coleoptile elongation, linoleic acid, oleic acid, and stearic acid, fatty acids with a lesser extent of unsaturation, had no such effects. The effects of lysophosphatidylcholine, linolenic acid, and arachidonic acid on H + secretion were not additive to that of indoleacetic acid (IAA), suggesting that lysophospholipids, fatty acids and auxin use similar pathways for the activation of the H + ‐pump. The phospholipase A 2 inhibitors, aristolochic acid and manoalide, inhibited the IAA‐induced pH o decrease and coleoptile elongation. The general protein kinase inhibitors, H‐7 or staurosporine, blocked the IAA‐ or lysophosphatidylcholine‐induced decrease in pH o . H‐7 also inhibited the coleoptile elongation induced by IAA or lysophosphatidylcholine. These results support the hypothesis that phospholipase A is activated by auxin, and that the products of the enzyme, lysophospholipids and fatty acids, induce acidification of the apoplast by activating the H + ‐pump through a mechanism involving a protein kinase, which in turn promotes com coleoptile elongation.