Beschreibung:
<jats:title>Summary</jats:title><jats:p>2,4‐dichlorophenoxyacetic acid (2,4‐D), a chemical analogue of indole‐3‐acetic acid (IAA), is widely used as a growth regulator and exogenous source of auxin. Because 2,4‐D evokes physiological and molecular responses similar to those evoked by IAA, it is believed that they share a common response pathway. Here, we show that a mutant, <jats:italic>antiauxin resistant1</jats:italic> (<jats:italic>aar1</jats:italic>), identified in a screen for resistance to the anti‐auxin <jats:italic>p</jats:italic>‐chlorophenoxy‐isobutyric acid (PCIB), is resistant to 2,4‐D, yet nevertheless responds like the wild‐type to IAA and 1‐napthaleneacetic acid in root elongation and lateral root induction assays. That the <jats:italic>aar1</jats:italic> mutation alters 2,4‐D responsiveness specifically was confirmed by analysis of GUS expression in the <jats:italic>DR5:GUS</jats:italic> and <jats:italic>HS:AXR3NT‐GUS</jats:italic> backgrounds, as well as by real‐time PCR quantification of <jats:italic>IAA11</jats:italic> expression. The two characterized <jats:italic>aar1</jats:italic> alleles both harbor multi‐gene deletions; however, 2,4‐D responsiveness was restored by transformation with one of the genes missing in both alleles, and the 2,4‐D‐resistant phenotype was reproduced by decreasing the expression of the same gene in the wild‐type using an RNAi construct. The gene encodes a small, acidic protein (SMAP1) with unknown function and present in plants, animals and invertebrates but not in fungi or prokaryotes. Taken together, these results suggest that SMAP1 is a regulatory component that mediates responses to 2,4‐D, and that responses to 2,4‐D and IAA are partially distinct.</jats:p>