Research article Isolation and characterization of a novel potato Auxin/Indole-3-Acetic Acid family member (StIAA2) that is involved in petiole hyponasty and shoot morphogenesis B. Kloosterman * , R.G.F. Visser, C.W.B. Bachem Laboratory of Plant Breeding, Department of Plant Sciences, Graduate School of Experimental Plant Sciences, Wageningen University and Research Center, P.O. Box 386, 6700 AJ Wageningen, The Netherlands Received 7 March 2006; accepted 10 October 2006 Available online 03 November 2006 Abstract Auxin/indole-3-acetid acid (Aux/IAA) proteins are short-lived transcriptional regulators that mediate their response through interaction with auxin response factors (ARF). Although 29 Aux/IAA proteins have been identified in Arabidopsis thaliana, their individual functions are still poorly understood and are largely defined by observed growth defects in gain-of-function mutant alleles. Here we present the isolation and characterization of a novel Aux/IAA protein in potato (Solanum tuberosum) that is named StIAA2. Down regulation of StIAA2 results in dis- tinctive phenotypes that include, increased plant height, petiole hyponasty and extreme curvature of growing leaf primordia in the shoot apex. Gene expression analysis of transgenic plants with reduced StIAA2 transcript levels resulted in the identification of a number of genes with altered expression profiles including another member of the Aux/IAA gene family (StIAA). The phenotypes that were observed in the StIAA2 suppression clones can be associated with both common as well as unique functional roles among Aux/IAA family members indicating the importance of analyzing Aux/IAA expression in different plant species. © 2006 Elsevier Masson SAS. All rights reserved. Keywords: Aux/IAA protein; Solanum tuberosum; Hyponasty; Shoot morphogenesis 1. Introduction It is well known that auxins, mainly represented by indole- 3-acetic acid (IAA), are important in plant growth and devel- opmental processes through the regulation of auxin responsive gene expression [1]. In recent years, the regulatory components of auxin signaling have become more evident and have revealed the existence of a highly complex system of both early and late auxin responses (reviewed in [2–4]). Several genes involved in the regulation of auxin dependent transcrip- tion have been identified in which primary roles have been given to the auxin responsive factors (ARF) [5] and Aux/IAA protein family members [6]. ARF proteins can function as either transcriptional activa- tors or repressors that can bind to auxin responsive elements (AuxREs) found in promoters of auxin responsive genes through a specific DNA binding domain [7]. The Aux/IAA proteins are short-lived transcription factors that contain four highly conserved domains (referred to as domain I, II, III and IV). Aux/IAA proteins are thought to act as regulators of auxin-induced gene expression through heterodimerization of domains III and IV with ARF proteins thereby modifying ARF activity [3,8,9]. In this model, auxin regulates transcrip- tion by stimulating the degradation of the Aux/IAA proteins through interaction of the Aux/IAA protein with the ubiquitin protein ligase SCF TIR1 complex [10]. Given that in Arabidopsis 29 different Aux/IAA and 23 ARF proteins have been identified to date, the number of potential Aux/IAA–ARF interactions and the subsequent auxin responses possible in the different tissues of a plant are enormous. www.elsevier.com/locate/plaphy Plant Physiology and Biochemistry 44 (2006) 766–775 Abbreviations : ARF, auxin response factor ; Aux/IAA, auxin/indole-3- acetic acid ; LD, long day conditions ; NTS, non-tuberizing stolon tip ; qRT- PCR, quantitative reverse transcriptase-polymerase chain reaction ; SD, short day conditions. * Corresponding author. Tel.: +31 317 48 4875; fax: +31 317 48 3457. E-mail addresses: bjorn.kloosterman@wur.nl (B. Kloosterman), richard.visser@wur.nl (R.G.F. Visser), christian.bachem@wur.nl (C.W.B. Bachem). 0981-9428/$ - see front matter © 2006 Elsevier Masson SAS. All rights reserved. doi:10.1016/j.plaphy.2006.10.026