Initiating inhibition

A recent publication by Schellmann et al. (2002) in The EMBO Journal has provided important insights into the control of cell fate and pattern formation in plants. To study the underlying molecular mechanisms, the authors made use of the development of root hairs and trichomes in Arabidopsis thaliana. A. thaliana trichomes are large, unicellular structures that project out from the shoot epidermal surface and are thought to form a defence against herbivorous insects. Root hairs are specialized cells extending from the root epidermis and are important for water and mineral uptake. The positional cues that regulate the spacing of trichomes and root hairs are unique. In the root, positional information is derived from the location of the epidermal cells relative to underlying cortex cells (Fig. 1A). Epidermal cells that are located over a junction between two cortex cells become root hairs (H cells), whereas the other epidermal cells become non-root-hair cells (N cells). On the leaves, the trichome spacing pattern is determined largely by the position of the first trichome (Fig. 1B). After the leaf primordium reaches a length of ~100 μm, a single epidermal cell at the leaf tip becomes a trichome. Thereafter, a regulated spacing pattern evolves in which newly initiated trichomes are approximately equal distance from one another. As older trichomes become separated by epidermal cell divisions, new intervening trichomes emerge (Fig. 1B). Despite the obvious differences between these systems, extensive mutational analyses of root hair and trichome development have identified a partly shared set of genes encoding transcription factors that regulate the patterning of both cell types (see Table 1) (Szymanski et al., 2000; Dolan, 2001). These genes seem to act by promoting trichome development in the shoot, and inhibiting H-cell initiation in the root. They include the functionally equivalent Myb genes GLABROUS1 (GL1) and WEREWOLF (WER), which are expressed in the shoot and root, respectively; the WD-40 repeat-encoding gene TRANSPARENT TESTA GLABRA (TTG), which probably acts as a transcriptional scaffold in both the shoot and root; and the basic helix–loop–helix (bHLH) gene GLABRA3 (GL3). Although mutations in GL3 affect only trichome initiation, a closely related bHLH gene in A. thaliana is predicted to have overlapping functions with GL3 in both the root and shoot. Yeast interaction assays have shown that the GL3 protein can homodimerize and contains discrete domains that interact with the GL1 and TTG proteins (Payne et al., 2000). It has been proposed that a protein complex composed of GL1, GL3 and TTG functions as an activator of genes required for trichome formation and that a similar complex containing WER, TTG and a bHLH protein is important for N-cell identity. The homeodomain encoding GLABRA2 (GL2), which is required for both trichome differentiation and root hair repression, is likely to be a primary target of the shoot and root complexes. The expression patterns of WER, GL1 and GL2 have been well characterized. In the shoot, GL1 and GL2 are diffusely expressed throughout young leaf primordia before the emergence of trichomes, and increase sharply in incipient trichomes (Szymanski et al., 1998). In the root, the expression of WER and GL2 is largely restricted to the N cells (Lee & Schiefelbein, 1999). So how is the spacing of trichomes controlled? The gene TRIPTYCHON (TRY) is a key player, because mutations in TRY result in an abnormally high frequency of clustered trichomes (Hülskamp et al., 1994). Now, in this recent paper, Schellmann et al. report that TRY encodes another Myb-like transcription factor; however, unlike WER and GL1, which encode proteins with two Myb DNA-binding domains and putative acidic transcriptional activation domains, the predicted TRY protein contains only one Myb DNA-binding domain and seems to lack an activator domain. The expression pattern of TRY in the shoot mirrors the expression of GL1 and GL2. Given that the genes that positively influence trichome initiation (GL1 and GL2)