The Occurrence of Auxin-induced Pectin Methylation in Plant Tissues

Abstract

Treatment of coleoptile tissues with indoleacetic acid (IAA) lead to an enhanced incorporation of mnethyl groups into both the cold-water-soluble uronic acids (C-Pectin) and the hot-water-extractable fraction of the cell wall (HW-Pectin). This promotion of pectin methylation is one of the most extensively studied of the biochemical effects of auxin (4, 5, 7, 8, 9). There are 2 reasons for this particular attention. First, it is one of the few biochemical effects which has been shown to occur in response to auxin rather than to cell elongation. This is indicated by the fact that IAA still enhances pectin methylation even when all cell elongation is osmotically inhibited (9). Secondly, it was thought that this reaction might be important in the loosening of the cell wall and, thus, in auxin-induced cell elongation (8,9). This possibility has been eliminated by the finding that auxin-induced cell elongation can occur even when auxin-induced methylation is completely blocked by ethionine (5). Although this auxin-induced pectin methylation does not lead to cell elongation, it may still be important in the growth or development of cells. If this is so, one might expect to find this particular biochemical effect in most primary plant tissues. At present, auxin-induced pectin methylation has only been found in one highly specialized organ, the coleoptile of Avena and maize (4). The following investigation was carried out in order to determine whether auxin-induced pectin methylation is of common occurrence in plant tissues. Selected for study were tissues in which elongation is promoted by IAA (Avena coleoptile, maize coleoptile and mesocotyl, Helianthus hypocotyl, and pea epicotyl), insensitive to IAA (Avena leaf), or inhibited by IAA (pea root).