High impact information on AXR3

• We demonstrate that SCF(TIR1) interacts with AXR2/IAA7 and AXR3/IAA17, and that domain II of these proteins is necessary and sufficient for this interaction [1].
• Changes in diverse auxin responses result from mutations in the Arabidopsis AXR3 gene [2].
• Furthermore, hobbit mutants show a reduction in DR5 :: GUS auxin reporter gene expression and accumulate the AXR3/IAA17 repressor of auxin responses [3].
• Selectively disrupting the auxin responsiveness of expanding epidermal cells by expressing a mutant form of the AUX/IAA17 protein, axr3-1, abolished root gravitropism [4].
• Both sar1 and sar3 mutations affect the localization of the transcriptional repressor AXR3/INDOLE ACETIC ACID17, providing a likely explanation for suppression of the phenotype conferred by axr1 [5].

Biological context of AXR3

• IAA17/AXR3: biochemical insight into an auxin mutant phenotype [6].
• Mutant axr3 plants show enhanced apical dominance, reduced root elongation, increased adventitious rooting, no root gravitropism, and ectopic expression from the SAUR-AC1 promoter [7].
• Single amino acid substitutions of PSIAA6 in conserved domain II, equivalent to those found in two alleles of axr3, a gene that encodes Aux/IAA protein IAA17, resulted in a greater than 50-fold increase in protein accumulation [8].

Other interactions of AXR3

• AXR3 and SHY2 interact to regulate root hair development [9].
• Auxin regulates turnover of the related Auxin-resistant (AXR)2/IAA7 and AXR3/IAA17 proteins by increasing their interaction with the Skp1-Cdc53/cullin-F-box (SCFTIR1) E3 ubiquitin ligase complex [10].

References