The plant hormone auxin regulates various developmental processes including root formation, vascular development, and gravitropism. Mutations within the AUX1 gene confer an auxin-resistant root growth phenotype and abolish root gravitropic curvature. Polypeptide sequence similarity to amino acid permeases suggests that AUX1 mediates the transport of an amino acid-like signaling molecule. Indole-3-acetic acid, the major form of auxin in higher plants, is structurally similar to tryptophan and is a likely substrate for the AUX1 gene product. The cloned AUX1 gene can restore the auxin-responsiveness of transgenic aux1 roots. Spatially, AUX1 is expressed in root apical tissues that regulate root gravitropic curvature.

Shoot branching is inhibited by auxin transported down the stem from the shoot apex. Auxin does not accumulate in inhibited buds and so must act indirectly. We show that mutations in the MAX4 gene of Arabidopsis result in increased and auxin-resistant bud growth. Increased branching in max4 shoots is restored to wild type by grafting to wild-type rootstocks, suggesting that MAX4 is required to produce a mobile branch-inhibiting signal, acting downstream of auxin. A similar role has been proposed for the pea gene, RMS1. Accordingly, MAX4 and RMS1 were found to encode orthologous, auxin-inducible members of the polyene dioxygenase family.Supplemental material is available at http://www.genesdev. org.Received December 6, 2002; revised version accepted March 20, 2003. Variation in shoot branching is an important cause of diversity in plant form. Individual species have a characteristic branching pattern, which can change through the life cycle in response to developmental cues and to environmental conditions (Cline 1991;Beveridge et al. 2003). Branching control therefore requires the integration of many signals, both known and unknown.Shoot branches arise from axillary meristems that form in the axils of leaves on the primary shoot axis. The axillary meristems themselves initiate leaves to form a bud. Bud growth can arrest but has the potential to reactivate to produce a shoot branch. Removal of the primary shoot apex results in activation of arrested axillary buds. The ability of the shoot apex to repress axillary bud growth is termed apical dominance. Thimann and Skoog (1933) reported that a compound, derived from the shoot apex, and later identified as auxin (indole-3-acetic acid), could inhibit the growth of lateral buds when applied to the stump of a decapitated plant. Subsequent work has provided multiple lines of evidence in support of auxinmediated bud inhibition in planta. However, a second messenger must relay the auxin signal into the bud because apically derived auxin is not transported into buds (Morris 1977) and exogenous auxin applied directly to buds does not inhibit their growth (Cline 1996).One model proposes that the effect of auxin on bud growth is mediated by cytokinin. Cytokinin can directly promote bud growth (Cline 1991); transgenic plants with increased auxin levels have reduced cytokinin levels (Eklö f et al. 2000), and cytokinin export from roots increases after decapitation, with this increase being abolished by application of auxin to the decapitated stump (Bangerth 1994). However, there is also good evidence for novel regulators of bud growth downstream of auxin. The ramosus mutants (rms1 to rms5) of pea (for reviews, see Beveridge 2000; Beveridge et al. 2003) have increased lateral branching, but this phenotype can be almost completely rescued by grafting a wild-type (WT) rootstock to an rms1, rms2, or rms5 mutant scion. Such grafting studies show that RMS1 and RMS5 are required for the production of a graft transmissible signal that moves from root to shoot and inhibits branching ...

Nucleocytoplasmic transport of macromolecules is regulated by a large multisubunit complex called the nuclear pore complex (NPC). Although this complex is well characterized in animals and fungi, there is relatively little information on the NPC in plants. The suppressor of auxin resistance1 (sar1) and sar3 mutants were identified as suppressors of the auxin-resistant1 (axr1) mutant. Molecular characterization of these genes reveals that they encode proteins with similarity to vertebrate nucleoporins, subunits of the NPC. Furthermore, a SAR3-green fluorescent protein fusion protein localizes to the nuclear membrane, indicating that SAR1 and SAR3 are Arabidopsis thaliana nucleoporins. Plants deficient in either protein exhibit pleiotropic growth defects that are further accentuated in sar1 sar3 double mutants. Both sar1 and sar3 mutations affect the localization of the transcriptional repressor AXR3/INDOLE ACETIC ACID17, providing a likely explanation for suppression of the phenotype conferred by axr1. In addition, sar1 sar3 plants accumulate polyadenylated RNA within the nucleus, indicating that SAR1 and SAR3 are required for mRNA export. Our results demonstrate the important role of the plant NPC in hormone signaling and development.

Strigolactones (SLs) are hormonal signals that regulate multiple aspects of shoot architecture, including shoot branching. Like many plant hormonal signaling systems, SLs act by promoting ubiquitination of target proteins and their subsequent proteasome-mediated degradation. Recently, SMXL6, SMXL7, and SMXL8, members of the SMAX1-LIKE (SMXL) family of chaperonin-like proteins, have been identified as proteolytic targets of SL signaling in Arabidopsis thaliana. However, the mechanisms by which these proteins regulate downstream events remain largely unclear. Here, we show that SMXL7 functions in the nucleus, as does the SL receptor, DWARF14 (D14). We show that nucleus-localized D14 can physically interact with both SMXL7 and the MAX2 F-box protein in a SL-dependent manner and that disruption of specific conserved domains in SMXL7 affects its localization, SL-induced degradation, and activity. By expressing and overexpressing these SMXL7 protein variants, we show that shoot tissues are broadly sensitive to SMXL7 activity, but degradation normally buffers the effect of increasing SMXL7 expression. SMXL7 contains a well-conserved EAR (ETHYLENE-RESPONSE FACTOR Amphiphilic Repression) motif, which contributes to, but is not essential for, SMXL7 functionality. Intriguingly, different developmental processes show differential sensitivity to the loss of the EAR motif, raising the possibility that there may be several distinct mechanisms at play downstream of SMXL7. INTRODUCTIONShoot system architectural characteristics strongly influence the productivity of many crop species, and architectural traits have been selected in both historical and contemporary breeding schemes. Understanding the mechanisms that regulate shoot architecture, and its environmental responsiveness, is therefore an important goal for plant research. It is well established that long-distance hormonal signals, including auxin, cytokinin, and strigolactone (SL), are key regulators of shoot architecture and allow communication both within the shoot system and between the shoot and root . For instance, cytokinin produced in the root system in response to the availability of nitrate ions is systemically transported to the shoot, where it promotes branching (Kiba et al., 2011; Müller et al., 2015). Similarly, root-derived SL plays a key role in negatively regulating branching in response to low phosphate availability in the rhizosphere (Kohlen et al., 2011). However, our understanding of the molecular mechanisms that act downstream of these hormones to alter developmental processes in the shoot is currently limited. This is particularly true of SLs. Analysis of the phenotypes of SL biosynthesis and signaling mutants has revealed roles for SLs in the regulation of shoot branching, branching angle, plant height, stem thickness, and leaf blade elongation . The role of SLs in regulating shoot branching has been intensively studied, resulting in two contrasting, nonexclusive models for their mode of action. In the first, SLs are proposed to act locally in axill...