Background Exocytosis is integral to root growth: trafficking components of systems that control growth (e. are due to the shorter meristems but not to lengthened cell cycles. Additionally mutants demonstrate reduced anisotropic cell expansion in the elongation zone but not the meristematic zone resulting in shorter mature cells that are comparable in Rabbit Polyclonal to GAB2. shape to wild-type. As expected hypersensitivity to brefeldin A links the mutant root growth defect to altered vesicular trafficking. Several experimental approaches (e.g. dose-response measurements localization of signaling components) failed to identify aberrant auxin or brassinosteroid signaling as a primary driver for reduced root growth in exocyst mutants. Conclusions The exocyst participates in two spatially distinct developmental processes apparently by mechanisms not directly linked FTY720 to auxin or brassinosteroid signaling pathways to help establish root meristem size and to facilitate rapid cell expansion in FTY720 the elongation zone. Electronic supplementary material The online version of this article (doi:10.1186/s12870-014-0386-0) contains supplementary material FTY720 which is available to authorized users. [22]. The two functions of the exocyst i.e. as a landmark or as an exocytosis facilitator may be separable as suggested by the observation that small GTPases appear to differentially regulate these two roles of the exocyst in non-plant species [21]. The exocyst functions as a complex in plants [19 25 where it is intimately associated with the process of growth. Mutation of exocyst components is associated with aberrant tip growth in pollen tubes [27 28 decreased polarized growth of root hairs [29] reduced elongation of hypocotyls in dark grown seedlings [27] FTY720 dwarfism [29 30 altered root tracheary element development [31] and defects in cytokinesis [30 32 33 Recently the exocyst complex has been visualized in epidermal cells of the root meristematic elongation and maturation zones in Arabidopsis demonstrating that subunits of the exocyst complex dynamically dock and undock at the plasma membrane potentially creating sites for vesicle tethering and exocytosis [34 35 In addition the trafficking dynamics of the BRI1 brassinosteroid receptor and PIN auxin transporters in the root are altered in exocyst mutants with the PIN trafficking defect thought to underlie the compromised polar auxin transport in mutant FTY720 roots [36]. Another potential linkage of the exocyst and auxin is derived from characterization of a plasma membrane-localized scaffold protein Interactor of Constitutive active ROP 1 (ICR1) which is required to maintain the primary root meristem [37]. ICR1 interacts with both small ROP GTPases and the exocyst subunit SEC3 and also affects trafficking of PIN auxin transporters to and from the plasma membrane in Arabidopsis roots [37 38 Thus it is evident that this exocyst could play an important role in root growth with current data pointing toward functions in auxin and/or brassinosteroid signaling [36 38 We therefore sought to investigate the exocyst’s role within the integrated network of mechanisms that regulate and produce primary root growth in insertion mutations in genes encoding exocyst FTY720 components were evaluated including mutations in mutation has previously been described [29]. Many mutations in exocyst components do not result in a discernible single mutant phenotype (e.g. mutation combined with the mutation results in a synergistic defect in hypocotyl elongation [27] and the same combination shows a more severe root growth defect than the mutant alone (Physique?1A). There are three paralogs in the Arabidopsis genome but mutants of one of them and and gene driven by the pollen-specific promoter was transformed into and heterozygous seedlings. The construct rescued the pollen defect in the mutants allowing generation of seedlings homozygous for the mutation and these proved to be extremely dwarfed (Additional file 1: Physique S1). RT-PCR (data not shown) suggests that the promoter can drive low-level transcription in the sporophyte (as also shown by Van Damme [39]) such that these and homozygous lines probably do not represent complete nulls for SEC8. (For brevity these lines will be henceforth referred to merely as or lines.) Additional lines were generated by combining the or mutations which do not have an obvious phenotype in the sporophyte with the mutation. These combinations also synergistically inhibit hypocotyl elongation [27] and result in a severe dwarfism of the same order of magnitude as the line. Notably the various exocyst mutants and.