The Epidermal Monolayer as an Information Superhighway

One of the major stumbling blocks when analysing the contribution of the epidermis to plant growth is undoubtedly the fact that, at least in Arabidop-sis, much of the extra-vascular movement of auxin to the shoot meristem and to the margins of young organ primordia (termed acropetal transport for the purpose of this review) is restricted to the L1 cell layer. Acropetal Polar Auxin transport (PAT) in L1 cells is absolutely required for phyllotaxis and the initiation and outgrowth of defined organ primordia, as well as the subsequent patterning and development of vascular strands within organs (mediated by basipetal PAT in internal cells) (Scarpella et al. 2006) (reviewed in Tanaka et al. 2006). At least two of the key proteins required for auxin transport in the apical meristem, the PIN1 efflux carrier and the AUX1 influx carrier, are primarily localized in the L1 cell layer in the shoot meristem and leaf primor-dia (Reinhardt et al. 2003b). Thus, disrupting L1 integrity should disrupt both organ initiation and vascular development. Indeed defects in these processes are observed in some L1 identity mutants (above), although it is difficult to decide with certainty the causes of such phenotypes when meristem maintenance and leaf morphology are also compromised.

Relatively little work has been carried out to assess why acropetal PAT is localized to the shoot L1. This type of study is non-trivial given the fact that auxin and PAT themselves control expression of auxin transporters (reviewed in Tanaka et al. 2006). However, one obvious possibility is that the genes encoding the proteins responsible for PAT such as AUX1, PIN1 and the MDR/PGP subfamily of ABC transporters are predisposed to L1 expression due to the presence of tissue specific elements in their promoters. No elements (such as L1-boxes) which confer L1-specific expression in shoots are obvious in the promoters of these genes (GI unpublished data). Moreover, during the establishment of PAT during embryogenesis, expression of transporters such as PIN1 is not restricted to L1 cells until well after protodermal identity has been established (Friml et al. 2003). In addition, the same transporters required for acropetal PAT in the L1 are also required internally for basipetal PAT in the developing vasculature. However, auxin-mediated tran-scriptional regulation, at least of PIN protein expression appears to occur via an AUX/IAA dependent pathway. Because of the potentially auxin independent, or at least tissue/organ specific expression of components of this pathway (for example AUXIN RESPONSE FACTOR transcription factors) this may add a layer of cell-type or tissue-type specificity to the process (Vieten et al. 2005).

Another explanation of the L1-localization of acropetal PAT is that the intrinsic physical properties of the L1-layer somehow favour PAT in the L1 over PAT in underlying cells. As PAT positively regulates the expression of at least some the transporters responsible, this would lead to an effective restriction of auxin movement to the L1-cell layer without the need to invoke tissue specific expression. The epidermis is organized as a planar monolayer composed of cells with a precisely defined apical-basal polarity with respect to the plant surface, and tight lateral cell-cell junctions without nascent air spaces. This may play an important role in facilitating the efficient movement of auxin and subsequent up-regulation of transporter expression. The cell walls between neighbouring L1 cells may even have properties which facilitate the efficient apoplastic movement of auxin. The plant surface could also serve to effectively corral auxin in the epidermal layer giving rise to higher auxin concentrations, and thus PAT in epidermal cells. However, testing whether such factors are important is again technically difficult. Interestingly, expression of a maize homologue of the Arabidopsis auxin efflux carrier PIN1 is down regulated in maize crinkly4 mutants (see below), where L1 identity and organization appear to be compromised at the shoot apex (Kessler et al. 2006).

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