Abstract

Recognition and repair of damaged tissue are an integral part of life. The failure of cells and tissues to appropriately respond to damage can lead to severe dysfunction and disease. Therefore, it is essential that we understand the molecular pathways of wound recognition and response. In this review, we aim to provide a broad overview of the molecular mechanisms underlying the fate of damaged cells and damage recognition in plants. Damaged cells release the so-called damage associated molecular patterns to warn the surrounding tissue. Local signaling through calcium (Ca2+), reactive oxygen species (ROS), and hormones, such as jasmonic acid, activates defense gene expression and local reinforcement of cell walls to seal off the wound and prevent evaporation and pathogen colonization. Depending on the severity of damage, Ca2+, ROS, and electrical signals can also spread throughout the plant to elicit a systemic defense response. Special emphasis is placed on the spatiotemporal dimension in order to obtain a mechanistic understanding of wound signaling in plants.

Highlights

  • Plants are especially susceptible to damage as they are unable to run away when facing danger

  • This review provides a broad overview of the recent developments in molecular mechanisms with a focus on spatiotemporal dynamics in order to gain mechanistic understanding and to address open questions in the field of wound response in plants

  • OGs are relatively immobile in the plant vascular system and may act as a local signal; because polygalacturonase activity is induced systemically in response to wounding, OGs may amplify responses in undamaged leaves (Table 1; Bergey et al, 1999)

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Summary

Introduction

Plants are especially susceptible to damage as they are unable to run away when facing danger. OGs are relatively immobile in the plant vascular system and may act as a local signal; because polygalacturonase activity is induced systemically in response to wounding, OGs may amplify responses in undamaged leaves (Table 1; Bergey et al, 1999).

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