Wound response in plants

There are many forms of defense that plants use to respond to wounding events. There are physical defense mechanisms that some plants utilize, through structural components, like lignin and the cuticle.[1] The structure of a plant cell wall is incredibly important for wound responses, as both protect the plant from pathogenic infections by preventing various molecules from entering the cell.[1]

Plants are capable of activating innate immunity, by responding to wounding events with damage-associated Molecular Patterns (DAMPs).[1] Additionally, plants rely on microbe-associated molecular patterns (MAMPs) to defend themselves upon sensing a wounding event. There are examples of both rapid and delayed wound responses, depending on where the damage took place.

Plants have pattern recognition receptors (PRRs) that recognize MAMPs, or microbe-associated molecular patterns.[2] Upon entry of a pathogen, plants are vulnerable to infection and lose a fair amount of nutrients to said pathogen. The constitutive defenses are the physical barriers of the plant; including the cuticle or even the metabolites that act toxic and deter herbivores. Plants maintain an ability to sense when they have an injured area and induce a defensive response. Within wounded tissues, endogenous molecules become released and become Damage Associated Molecular Patterns (DAMPs), inducing a defensive response. DAMPs are typically caused by insects that feed off the plant.[2] Such responses to wounds are found at the site of the wound and also systemically. These are mediated by hormones.[1]

As a plant senses a wound, it immediately sends a signal for innate immunity.[3] These signals are controlled by hormones such as jasmonic acid, ethylene and abscisic acid. Jasmonic acid induces the prosystemin gene along with other defense related genes such as abscisic acid, and ethylene, contributing to a rapid induction of defense responses. Other physical factors also play a vital role in wound signaling, which include hydraulic pressure and electrical pulses. Most of these that are involved within wound signaling also function in signaling other defense responses. Cross-talk events regulate the activation of different roles.[3]

Sieve elements are very rich in sugars and various organic molecules. Plants don't want to lose these sugars when the sieve elements get damaged, as the molecules are a very large energy investment. The plants have both short-term and long-term mechanisms to prevent sieve element sap loss.[2] The short-term mechanism involves sap proteins, and the long-term mechanism involves callose, which helps to close the open channels in broken sieve plates.[2]

The main mechanism for closing damaged sieve elements involves P-proteins, which act as a plug in the sieve element pores. P-proteins essentially plug the pores that form in sieve elements.[2] They act as a stopper in the damaged sieve elements by blocking the open channels so that no additional sap or sugar can be lost.[2]

A longer-term solution to wounded sieve tube elements involves the production of callose at the sieve pores. Callose is a β-1,3 glucan synthesized by callose synthase, which is an enzyme that's localized within the plasma membrane. Callose gets synthesized after the sieve tube elements undergo damage and/or stress. The use of wound callose occurs when callose gets deposited following sieve element damage.[2] Wound callose is proven to first be deposited at the sieve plate pores, or the intracellular connections, where it then spreads to different regions.[2] Essentially, wound callose seals off the parts that were damaged, and separates them from the parts that are still healthy and not broken. Once the sieve elements get fixed, the callose is always dissipated by callose-hydrolyzing enzyme.[2] Callose is also synthesized during normal plant growth and development, and it typically responds to things like high temperatures, or allows the plant to prepare for more dormant seasons.[2]

When the sieve elements get damaged, the sap, sugar, and other molecules inside rush to the end that was damaged. If there was no mechanism to stop the sugars from leaking out the plant would lose an incredibly large amount of invested energy.[2]

Jasmonic acid (JA) is a plant hormone that increases in concentration in response to insect herbivore damage. The rise in JA induces the production of proteins functioning in plant defenses. JA also induces the transcription of multiple genes coding for key enzymes of the major pathways for secondary metabolites. Its structure and synthesis show parallels to oxylipins, which function in inflammatory responses.[2] JA is synthesized by the octadecanoid pathway, which is activated in response to wound-induced signals.[4] It is a derivative of the most rich fatty acid in the lipids of leaf membranes, alpha-linolenic acid. When plants experience mechanical wounding or herbivory, JA is synthesized de novo and induces genome-wide changes in gene expression.[5] JA travels through plants via the phloem, and accumulates in vascular tissue.[6] JA acts as an intracellular signal in order to promote responses in distal tissues.[6] The perception of jasmonate in distal responding leaves is necessary for recognition of the transmissible signal that coordinates responses to wounding stress.[5] JA mutants, which lack the gene encoding jasmonic acid, are killed by insect herbivore damage that would otherwise not harm normal-type plants. Upon the application of JA to the same mutants, resistance is restored.[7] Signaling agents such as ethylene, methyl salicylate, and salicylic acid can pair with JA and enhance JA responses.[7]

• Embryo rescue
• Somatic embryogenesis
• Wound healing
• Jasmonic acid
• Herbivore
• Trichome
• Cuticle
• Pathogen