pax1-1 partially suppresses gain-of-function mutations in Arabidopsis AXR3/IAA17

We present the isolation of the partial suppressor of axr3-1 (pax1-1) mutant, which partially suppresses almost every aspect of the axr3-1 phenotype, and that of the weaker axr3-3 allele. axr3-1 protein turnover does not appear to be altered by pax1-1. However, expression of an AXR3::GUS reporter is reduced in a pax1-1 background, suggesting that PAX1 positively regulates AXR3 transcription. The pax1-1 mutation also affects the phenotypes conferred by stabilising mutations in other Aux/IAA proteins; however, the interactions are more complex than with axr3-1.We propose that PAX1 influences auxin response via its effects on AXR3 expression and that it regulates other Aux/IAAs secondarily.The phytohormone auxin is central to the regulation of plant growth and development. Processes controlled by auxin include apical dominance, adventitious root formation, tropic responses, vascular patterning and root hair development [1-6]. These diverse morphological events are brought about by changes in cell division, expansion and differentiation [7-9], and many of them are mediated by the ability of auxin to control gene expression. Several families of genes containing Auxin Response Elements (AuxREs) in their promoters, are rapidly transcriptionally upregulated as a primary response to auxin [10], including members of the Aux/IAA gene family.The Aux/IAA genes form a large multi-gene family found throughout the plant kingdom [11-14]. There are 29 members in Arabidopsis and their expression varies with respect to tissue specificity, auxin induction kinetics and sensitivity to auxin dose [11,15]. Aux/IAA proteins are characterised by four highly conserved domains [11]. C-terminal domains III and IV mediate homo- and hetero-dimerisation between Aux/IAA proteins [16]. Domains III and IV are also found in the Auxin Response Factor (ARF) family of transcription factors, a subset of which activate transcription from AuxRE-containing promoters [17,18]. Conservation of domains III and IV