Exogenous ethylene inhibits root elongation in different plant species. This was shown for Arabidopsis (reviewed by Bleecker et al. 1988; Smalle et al. 1997), cucumber (Pierik et al. 1999), and Rumex (Visser et al. 1997). This inhibition of elongation is at least partially dependent on an ethylene-induced inhibition of cell elongation. In Arabidopsis, wild-type epidermal cells with a visible root hair bulge (the first sign of root hair outgrowth) are shorter when treated with ACC or ethylene (Le et al. 2001). eto2 roots show this phenotype too (De Cnodder et al. 2005). Wild-type epidermal cells from plants treated with AVG (aminoethoxyvinylglycine, ACC synthase inhibitor) are larger than those of untreated seedlings (Le et al. 2001). This inhibition of elongation can be partly explained by a callose deposition in epidermis and cortex cells in the elongation and differentiation zone under the influence of ACC (De Cnodder et al. 2005). Since callose is a structural component of plasmodesmata (Roberts and Oparka 2003), it is possible that cell-to-cell transport is also part of the control mechanism for cell elongation. ACC also raises the hydrogen peroxide concentration (by NADPH oxidases), leading to cross-linking of hydroxyproline-rich glycoproteins (HRPG) in the cell wall by the oxidation of a tyrosine residue (De Cnodder et al. 2005), which presumably restricts cell wall extensibility.
To achieve root-growth inhibition, both ethylene and auxin are required. This is illustrated by the phenotype of wei-mutants (weak ethylene insensitive). Root elongation of dark-grown wei2 (Alonso et al. 2003) and wei7 (Stepanova et al. 2005) seedlings is not inhibited upon the application of ethylene. Nevertheless these mutants display a short hypocotyl and an exaggerated hook upon ethylene treatment, indicating uncoupling of different triple response phenotypes. Wez'2 is an allele of ASA1 (anthranilate synthase a), necessary for Trp synthesis. A previously identified mutant in this gene, tir7 (transport inhibitor response), is resistant to auxin transport inhibitors (Ljung et al. 2005). The effect of wei7 is caused by a mutation in ASB1 (anthranilate synthase ft). Both genes are expressed in the columella of roots and their expression is enhanced when ethylene is present. Applying ethylene to wild-type plants increases the expression of DR5-GUS (synthetic auxin reporter) in the root cap (Stepanova et al. 2005). DR5-GUS activity has been shown to correlate well with endogenous auxin levels in roots (Casimiro et al. 2001; Benkova et al. 2003). An ethylene-regulated increase in DR5-GUS expression is absent in ein2-5, wei2 and wei7, which is indicative of a lower IAA (indole-3-acetic acid) content, resulting in a longer root (Stepanova et al. 2005). Further proof of the need for both auxin and ethylene in the inhibition of root growth is delivered by wei1. This mutation is an allele of TIR1, lacking 21 carboxy terminal amino acids (Alonso et al. 2003). TIR1 normally interacts with the AUX/IAA proteins AXR2/IAA7 (auxin resistant) and AXR3/IAA17, labeling them for ubiquitin-dependent degradation and subsequent regulation of auxin-regulated genes (Gray et al. 2001). In wei1, ubiquitin labeling of AUX/IAA is abolished, blocking auxin response and hence conferring a longer root than that of the wild type when treated with ethylene or auxin.
Furthermore, upon treatment with ethylene, ARF19 (auxin response factor) expression increases (Li et al. 2006). Loss-of-function mutants in this gene have ethylene-insensitive roots. It is not yet clear whether this is a direct effect of ethylene on the expression of ARF19 or a consequence of the ethylene-dependent rise in IAA concentration.
It can be concluded that the addition of ethylene results in the inhibition of root elongation, an effect that is largely mediated by a change in auxin concentration and/or auxin signaling.
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