Abstract
SlARF2a is expressed in most plant organs, including roots, leaves, flowers and fruits. A detailed expression study revealed that SlARF2a is mainly expressed in the leaf nodes and cross-sections of the nodes indicated that SlARF2a expression is restricted to vascular organs. Decapitation or the application of 6-benzylaminopurine (BAP) can initially promote axillary shoots, during which SlARF2a expression is significantly reduced. Down-regulation of SlARF2a expression results in an increased frequency of dicotyledons and significantly increased lateral organ development. Stem anatomy studies have revealed significantly altered cambia and phloem in tomato plants expressing down-regulated levels of ARF2a, which is associated with obvious alterations in auxin distribution. Further analysis has revealed that altered auxin transport may occur via altered pin expression. To identify the interactions of AUX/IAA and TPL with ARF2a, four axillary shoot development repressors that are down-regulated during axillary shoot development, IAA3, IAA9, SlTPL1 and SlTPL6, were tested for their direct interactions with ARF2a. Although none of these repressors are directly involved in ARF2a activity, similar expression patterns of IAA3, IAA9 and ARF2a implied they might work tightly in axillary shoot formation and other developmental processes.
Highlights
SlARF2a is expressed in most plant organs, including roots, leaves, flowers and fruits
A glutamine-rich middle regions (MRs) acts as a transcriptional activator, whereas a proline and serine-rich MR acts as a transcriptional repressor[6,7]
The auxin reporter DR5 appeared in the radicle, whereas SlARF2a::GUS strictly appeared in the cotyledon (Fig. 1b,c)
Summary
SlARF2a is expressed in most plant organs, including roots, leaves, flowers and fruits. The transcriptional function of ARF is repressed by direct interactions with Aux/IAA proteins[9,10,11]. When auxin concentrations are high, TIR1/AFB interacts with the Skp1–Cullin–F-box (SCF) E3 ubiquitin ligase[4,12] to polyubiquitylate and target the Aux/IAA protein for degradation via the ubiquitin-mediated protein degradation pathway; subsequently, the repression on the ARF transcription factor is relieved and active auxin-dependent gene expression occurs[10,13,14]. TPL cooperates with AUX/IAA proteins by binding the activating ARF to suppress the expression of auxin-responsive genes under low concentrations of auxin[16,17]. The arf[7] arf[19] double mutant shows a more visible auxin-related phenotype not observed in arf[7] or arf[19] single mutants, with abolished lateral root development and hypocotyl gravitropism[19,28]
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