Auxin-Promoted Transport of Metabolites in Stems ofPhaseolus vulgarisL.: FURTHER STUDIES ON EFFECTS REMOTE FROM THE SITE OF HORMONE APPLICATION

Abstract

i v L) u i iv n v_^ x The proposal that indol-3yl-acetic acid (IAA) regulates acropetal transport in stems by acting along the transport channel was further investigated using decapitated seedlings of Phaseolus vulgaris. Concentrations of two inhibitors of auxin transport, which did not interfere with IAA-promoted basipetal transport, were found to decrease the IAA-promoted component of acropetal metabolite movement. This latter inhibition was relieved by treating the stems with a supplementary supply of IAA below the point of inhibitor application. These observations, together with the finding that the response time of transport to hormone action was strongly dependent on the distance over which IAA needed to move to be present throughout the length of the transport channel, provide support for the above proposed mode of IAA action. INTRODUCTION The previous paper in this series (Patrick and Wareing, 1978) described an attempt to ascertain the site (localized v. remote) of indol-3yl-acetic acid (IAA) stimulation of acropetal metabolite transport in decapitated stems of Phaseolus vulgaris L. seedlings. Adopting an approach pioneered by Davies and Wareing (1965), these possible action sites were isolated experimentally using the auxin-transport inhibitor, 2,3,5-triiodobenzoic acid (TIBA), applied midway along the decapitated internode. Under these conditions a TIBA-induced reduction in the IAA-promoted component of acropetal assimilate flow was associated with a TIBA inhibition of basipetal IAA movement (Patrick and Wareing, 1978). Moreover, it was found that by applying IAA below the TIBA ring IAA-promoted transport was restored. On this evidence, it was argued that IAA-promoted acropetal transport depended on stem levels of IAA distant from the point of hormone application. However, whilst TIBA appeared to act specifically on IAA-promoted acropetal transport (Patrick and Wareing, 1978), the possibility of some effect unrelated to inhibition of auxin transport could not be ruled out unequivocally. Based on these considerations, and the need to subject the problem to other experimental approaches, further studies were undertaken. Essentially, the critical TIBA experiments were repeated using two inhibitors of auxin transport (viz. l-(2 This content downloaded from 207.46.13.128 on Wed, 07 Sep 2016 06:03:22 UTC All use subject to http://about.jstor.org/terms 2 Patrick—Auxin-Promoted Transport carboxyphenyl)-3-phenylpropane-l,3-dione (ACP1.55) and eosin (Katekar and Geissler, 1975)). Unlike TIBA, which is an auxin competitor (cf. Gaither and Abeles, 1975), these two inhibitors are considered to interfere with IAA action solely through their capacity to inhibit polar auxin transport (Katekar, personal communication) and, as such, are ideally suited to regulate specifically IAA levels in decapitated stems. Another approach was based on the premise that, if IAA promotion of acropetal metabolite transport was dependent on the presence of IAA at remote sites along the transport pathway, then the lag period (i.e. duration between application of IAA and onset of promoted assimilate flow) should be a function of the distance over which IAA must move to reach these sites. MATERIALS AND METHODS