Plants react to wounding and herbivory by activating complex signalling pathways that lead to transcriptional reprogramming at the damaged leaf and at distal, undamaged ones. Signalling involves the perception of both damaged‐self and herbivore‐derived elicitors, and may be modulated by insect oral secretions. Systemic transmission of the signal occurs along the vasculature, and involves membrane depolarisation and hydraulic waves. An increase in jasmonic acid (JA)‐Ile synthesis is a hallmark of damage. JA‐Ile binding by the COI1‐JAZ receptor complex results in degradation of JAZ repressors, thereby releasing transcription factors that activate local and systemic defence gene expression. There is little overlap between the set of genes induced in the damaged leaf and that in distal, undamaged ones. Whereas genes induced locally are largely devoted to wound healing and limiting further desiccation, many of those induced systemically produce defensive proteins that reduce the nutritional value of the tissue, in anticipation of subsequent herbivore attack.
- Plants have an intrinsic response to damage that triggers transcriptional reprogramming.
- Wounding releases plant‐derived damage‐associated molecular patterns (DAMPs).
- Herbivory activates the plant's response to damage, which is modulated by herbivore‐derived elicitors and oral secretions.
- Damage‐responsive genes are induced close to the wounds and in distal, undamaged tissues.
- Damage signals generated at the wound site travel along the vasculature to trigger a systemic defence response.
- Synthesis and perception of JA‐Ile is key for wound‐induced gene expression.
- JA‐Ile binding to the COI1/JAZ receptor complex triggers degradation of JAZ repressors, thereby releasing transcription factors that regulate wound‐responsive gene expression.
Keywords: damage; herbivory; DAMPs; wound signals; jasmonic acid; COI1/JAZ receptor; defence gene expression