Many plant species respond to damage from herbivore grazing by generating leaves with more trichomes (hair-like epidermal cells). Interestingly, damage at mature leaves affects newly forming leaf primordia and increases the frequency with which epidermal cells adopt a trichome fate. What controls this fate choice systemically? The answer, report Kiyotaka Okada and co-workers on , is the plant hormone jasmonic acid. In Arabidopsis mutants that lack endogenous jasmonate (JA) signalling, trichome formation is normal, but the trichome patterning wounding response is absent. The authors isolate two additional wounding response mutants, unarmed 9 (urm9) and urm23 (which is allelic to ttg1). In both mutants, the subnuclear localisation of the bHLH transcription factor GLABRA3 (GL3), a component of the Myb-bHLH-WD40 complex that regulates trichome development, is disrupted. In addition, JA treatment enhances GL3 expression prior to trichome initiation in both wild-type and urm9 backgrounds. Based on these and other results, the authors propose that the activation of GL3 by JAs constitutes the link between the wounding response and trichome patterning in Arabidopsis.
