The rib1 Mutant Is Resistant to Indole-3-Butyric Acid, an Endogenous Auxin in Arabidopsis

Abstract

The presence of indole-3-butyric acid (IBA) as an endogenous auxin in Arabidopsis has been recently demonstrated. However, the in vivo role of IBA remains to be elucidated. We present the characterization of a semi-dominant mutant that is affected in its response to IBA, but shows a wild-type response to indole-3-acetic acid (IAA), the predominant and most studied form of auxin. We have named this mutant rib1 for resistant to IBA. Root elongation assays show that rib1 is specifically resistant to IBA, to the synthetic auxin 2,4-dichlorophenoxyacetic acid, and to auxin transport inhibitors. rib1 does not display increased resistance to IAA, to the synthetic auxin naphthalene acetic acid, or to other classes of plant hormones. rib1 individuals also have other root specific phenotypes including a shortened primary root, an increased number of lateral roots, and a more variable response than wild type to a change in gravitational vector. Adult rib1 plants are morphologically indistinguishable from wild-type plants. These phenotypes suggest that rib1 alters IBA activity in the root, thereby affecting root development and response to environmental stimuli. We propose models in which RIB1 has a function in either IBA transport or response. Our experiments also suggest that IBA does not use the same mechanism to exit cells as does IAA and we propose a model for IBA transport.

Mutations in an Auxin Receptor Homolog AFB5 and in SGT1b Confer Resistance to Synthetic Picolinate Auxins and Not to 2,4-Dichlorophenoxyacetic Acid or Indole-3-Acetic Acid in Arabidopsis

“…This pathway has been shown to be the signal transduction mechanism for plant responses to 2,4-D and IAA (Leyser, 2002;Dharmasiri and Estelle, 2004). Although other auxin-resistant mutants such as rib1, aux1, and eir1 have been observed to have some chemical specificity, their differential resistance is due to the specificity of pumps and cellular uptake mechanisms (Yamamoto and Yamamoto, 1998;Marchant et al, 1999;Poupart and Waddell, 2000) rather than in components of auxin signal transduction. None of the three examples of mutants within the auxin signal transduction pathway that we tested, tir1, axr1, and axr2, displayed the marked chemical selectivity in responses that we observed with afb5 and sgt1b.…”

The rib1 Mutant of Arabidopsis Has Alterations in Indole-3-Butyric Acid Transport, Hypocotyl Elongation, and Root Architecture

“…The auxin activity of IBA is well recognized, as it has long been used as the auxin of choice for root formation on cuttings (Zimmerman and Wilcoxon, 1935;Hartmann et al, 1997). Like the auxin indole-3-acetic acid (IAA), IBA affects lateral root induction and elongation of roots, shoots, and hypocotyls (Yang and Davies, 1999;Poupart and Waddell, 2000;Zolman et al, 2000;Rashotte et al, 2003).…”

“…Several studies have demonstrated that internal IBA levels, not IAA levels, increase and stay elevated during IBA-induced root formation (Nordstrom et al, 1991;van der Krieken et al, 1992). The occurrence of several IBA-resistant, IAA-sensitive mutants that do not have defects in b-oxidation also suggest that IBA could act directly, and not necessarily through conversion to IAA (Poupart and Waddell, 2000;Zolman et al, 2000). Polar auxin transport is a specialized delivery system that moves IAA from its point of synthesis in young apical tissues to the rest of the plant in a highly regulated manner .…”

“…rib1 was isolated in a screen for mutants with defects in root gravitropism and shown previously to have an altered response when the root is reoriented with respect to the gravity vector (Poupart and Waddell, 2000). Further characterization of the mutant revealed it was less sensitive to root elongation inhibition by the auxins IBA and 2,4-D, but had a wild-type response to IAA and the synthetic auxin NAA.…”

“…Adult rib1 plants, however, were indistinguishable from the wild type in terms of shoot length and secondary inflorescence formation. Based on its phenotypes and the resistance of rib1 to IAA efflux inhibitors, we had hypothesized that this mutant could be defective in IBA transport or response (Poupart and Waddell, 2000).…”