Trichomes are epidermal structures that often resemble hairs that grow in regular patterns on various parts of plants. Although most models of trichome patterning invoke an activation-inhibition mechanism, Bouyer et al . suggest that a trapping-depletion mechanism may also be important. The activation-inhibition mechanisms involve the formation of an active trimeric complex of a single R2R3 MYB transcription factor (GL1 or MYB23), the WD40 repeat protein TTG1, and a basic helix-loop-helix (bHLH) transcription factor (GL3 or EGL3). The inhibitor is an R3 MYB-like transcription factor (TRY, CPC, ETC1, ETC2, TRICHOMELESS1, or CPL3) that competes with the R2R3 MYB-TTG1 complex for binding to the bHLH transcription factor. Bouyer et al . expressed a yellow fluorescent protein (YFP)-tagged TTG1 (TTG1-YFP) under control of the TTG1 promoter and found that the protein was ubiquitously distributed in young leaves before trichome formation, but as trichome formation began, TTG1-YFP accumulated in the incipient trichome cells and was less abundant in the neighboring cells, with those closest to the trichome having the least and abundance increasing with distance from the trichome. Inhibition of the proteasome by exposure of the plants to epoxomicin did not prevent this pattern of high and low TTG1-YFP abundance in the leaf cells, but did allow TTG1 to accumulate in the cotyledons, in which TTG1-YFP was undetectable in the absence of proteasomal inhibition. TTG1 appeared to move between cells, likely through plasmodesmata (selective pores between plant cells). When TTG1-YFP was expressed by a promoter that did not drive expression in trichome cells, TTG1-YFP appeared in the initiating trichomes. In mosaic leaves in which the TGG1 gene was selectively knocked out in some regions, trichomes formed even in the null areas. After microinjection of tagged TTG1 into a tobacco mesophyll cell, TTG1 appeared in neighboring cells, and TTG1-YFP appeared in epidermal cells when expression was forced in subepidermal cells, which are connected to the epidermal cells by plasmodesmata. In plants deficient for GL3, TTG1-YFP was slightly higher in the incipient trichome cell, but was not substantially depleted from the neighboring cells. The authors propose that GL3, which is more abundant in trichome cells, presumably through a transcriptional positive feedback mechanism, binds TTG1 in the initiating trichome; thus, as TTG1 moves out of the adjacent cells, it is trapped in the GL3-positive cells that form the trichome. Mathematical modeling of trapping-depletion-mediated trichome patterning provided a mechanism by which null alleles result in a glabrous (trichomeless) phenotype, but weak alleles lead to clustering of trichomes. D. Bouyer, F. Geier, F. Kragler, A. Schnittger, M. Pesch, K. Wester, R. Balkunde, J. Timmer, C. Fleck, M. Hülskamp, Two-dimensional patterning by a trapping/depletion mechanism: The role of TTG1 and GL3 in Arabidopsis trichome formation. PLoS Biol. 6 , e141 (2008). [PubMed]