AUX/LAX family of auxin influx carriers-an overview

Abstract

Auxin regulates several aspects of plant growth and development. Auxin is unique among plant hormones for exhibiting polar transport. Indole-3-acetic acid (IAA), the major form of auxin in higher plants, is a weak acid and its intercellular movement is facilitated by auxin influx and efflux carriers. Polarity of auxin movement is provided by asymmetric localization of auxin carriers (mainly PIN efflux carriers). PIN-FORMED (PIN) and P-GLYCOPROTEIN (PGP) family of proteins are major auxin efflux carriers whereas AUXIN1/LIKE-AUX1 (AUX/LAX) are major auxin influx carriers. Genetic and biochemical evidence show that each member of the AUX/LAX family is a functional auxin influx carrier and mediate auxin related developmental programmes in different organs and tissues. Of the four AUX/LAX genes, AUX1 regulates root gravitropism, root hair development and leaf phyllotaxy whereas LAX2 regulates vascular development in cotyledons. Both AUX1 and LAX3 have been implicated in lateral root (LR) development as well as apical hook formation whereas both AUX1 and LAX1 and possibly LAX2 are required for leaf phyllotactic patterning.

Keywords: AUX1; AUXLAX; LAX1; LAX2; LAX3; auxin; auxin transport; influx carriers.

Figure 1

Auxin chemical properties and chemioosmotic hypothesis of auxin transport. The percentages of the anionic and protonated forms of IAA (indole acetic acid) are given as a funtion of pH with an emphasis on the apoplastic and cytosolic pH ranges (A). Chemiosmotic auxin transport model showing the different families of transporters: AUX/LAX, PIN, and PGP. The artificial form of auxin 1-NAA (1-Naphthalene acetic acid) is lipophilic and diffuses freely inside the cell (B).

Figure 2

The AUX/LAX family of auxin influx transporters. Genetic organization of the AUX/LAX genes sequences showing exons (gray boxes) and introns (bars) (Péret et al., 2012) (A). Phylogenetic tree of the AUX/LAX protein sequences generated from a ClustalW alignment (B). Percentage of identity between the members of the AUX/LAX family (identity is given a the score returned upon the ClustalW alignment) (C).

Figure 3

Mutations in AUX/LAX genes result in auxin related developmental defects. AUX1 regulates root gravitropism (Swarup et al., 2001, 2004, 2005). AUX1 is expressed in tissues that are involved in gravity perception, signal transmission, and response and mutation in aux1 cause agravitropic roots (A). Both AUX1 and LAX3 regulate lateral root development (Swarup et al., 2008). AUX1 is expressed in lateral root primordia whereas LAX3 in the cortical and epidermal cells in contact with the primordia and aux1 lax3 double mutants have severely delayed lateral root emergence (B). LAX2 regulates vascular patterning in cotyloedons (Péret et al., 2012). LAX2 is expressed in the vascular tissues during embryo development and lax2 mutants show vascular breaks in the cotyledons (C). (Scale bars 20 μm).

Figure 4

Lateral root are formed within the pericycle deep inside the primary root and have to emerge through the outer tissue, passing through the endodermal, cortical (blue), and epidermal cells (A). Mechanism proposed by Swarup et al. (2008) describing how auxin (IAA) entering the cortical cell induces the expression of LAX3. This generates the establishment of a positive feedback loop that triggers high auxin levels and subsequent induction of cell wall remodeling (CWR) genes, such as the polygalacturonase (PG) (B).

Figure 5

Auxin influx transporters are involved in biotic interactions. During the actinorhizal symbiosis, Frankia infects the plant cell and triggers the expression of CgAUX1, resulting in auxin (IAA) uptake by the plant. Auxin is presumably synthesized by the actinobacteria (Péret et al., 2007) (A). During cyst nematode infection, effector proteins are released in the plant cell. The 19C07 protein has been shown to directly interact with LAX3. High expression levels of LAX3 in the feeding site and adjacent cells participates in the incorporation of these cells in the feeding sites by promoting cell wall remodeling (CWR) (Lee et al., 2011) (B).