Auxin-binding proteins of Zea mays identified by photoaffinity labelling.

Auxins [indole-3-acetic acid (IAA) and related natural and synthetic analogues] are a group of phytohormones that influence fundamental growth and development responses in plants, e.g. cell elongation and cell division (see [l] for review). It is thought tht auxins are synthesized in apical meristems and move by polar transport to basal/subapical target tissues. The control of auxin concentrations in different tissues is assumed to be mediated by synthesis, oxidative decomposition, conjugation, compartmentalization and transport, the latter being mediated by carrier proteins [2]. However, little is known of the molecular events of auxin action and control. Auxin perception and the ensuing responses are thought to be mediated initially by auxin receptors. Binding and inhibitor studies have identified auxin-binding sites located in (i) the endoplasmic reticulum, (ii) the tonoplast and (iii) plasma membrane [3]. An auxin-binding protein (ER-abp 1) identified first in the endoplasmic reticulum has been purified and its primary structure deduced [4]. Work in several laboratories including our own, and described elsewhere in this volume, suggests that ER-abpl or a related protein may be a receptor for the auxin signal at the endoplasmic reticulum or plasma membrane. Auxin-binding sites on the plasma membrane have been implicated recently in perception of the auxin signal (see Barbier-Brygoo et aL, pp. 59-63 this volume), but are also thought to be involved in the transport of auxin across the membrane [5]. Auxin transport in shoot tissues seems to involve a saturable, specific nH+/IAAinflux carrier although passive uptake of undissociated IAA also occurs [Z, 51. The efflux carrier is inhibited by polar-auxin-transport inhibitors, e.g. 2,3,5-triiodobenzoic acid (TIBA) and the phytotropin 1-Nnaphthylphthalamic acid (NPA); responses in vivo to NPA correlate with inhibition in vitro of auxin eMux from plasma membrane vesicles, which were found to have increased net accumulation of IAA [5, 61.