Plants undergoing the onslaught of wound‐causing agents activate mechanisms directed to healing and further defence. Responses to mechanical damage are either local or systemic or both and hence involve the generation, translocation, perception, and transduction of wound signals to activate the expression of wound‐inducible genes. Although the central role for jasmonic acid in plant responses to wounding is well established, other compounds, including the oligopeptide systemin, oligosaccharides, and other phytohormones such as abscisic acid and ethylene, as well as physical factors such as hydraulic pressure or electrical pulses, have also been proposed to play a role in wound signalling. Different jasmonic acid‐dependent and –independent wound signal transduction pathways have been identified recently and partially characterized. Components of these signalling pathways are mostly similar to those implicated in other signalling cascades in eukaryotes, and include reversible protein phosphorylation steps, calcium/calmodulin‐regulated events, and production of active oxygen species. Indeed, some of these components involved in transducing wound signals also function in signalling other plant defence responses, suggesting that cross‐talk events may regulate temporal and spatial activation of different defences.

Read the full review for this F1000Prime recommended article: CLV3 is localized to the extracellular space, where it activates the Arabidopsis CLAVATA stem cell signaling pathway.

Stress constantly challenges plant adaptation to the environment. Of all stress types, arsenic was a major threat during the early evolution of plants. The most prevalent chemical form of arsenic is arsenate, whose similarity to phosphate renders it easily incorporated into cells via the phosphate transporters. Here, we found that arsenate stress provokes a notable transposon burst in plants, in coordination with arsenate/phosphate transporter repression, which immediately restricts arsenate uptake. This repression was accompanied by delocalization of the phosphate transporter from the plasma membrane. When arsenate was removed, the system rapidly restored transcriptional expression and membrane localization of the transporter. We identify WRKY6 as an arsenate-responsive transcription factor that mediates arsenate/phosphate transporter gene expression and restricts arsenate-induced transposon activation. Plants therefore have a dual WRKY-dependent signaling mechanism that modulates arsenate uptake and transposon expression, providing a coordinated strategy for arsenate tolerance and transposon gene silencing.