Fig. 2

Schematic diagram of partial DAMPs signal transduction. After cell damage, glutamate and ATP, which are cell contents, dissociate in the periplasmic space. They then bind to nearby cells membrane receptors, such as GLR and P2K1, resulting in the influx of Ca²⁺ and triggering the efflux of Cl- to polarize cells and create a potential difference. Depolarization is achieved by draining H+ through the AHA1 receptor channel. It has been proposed that H+ can also promote depolarization by acting on GLR. Simultaneously, second messengers like Ca²⁺ are transmitted to peripheral cells through plasmodesmata, leading to the generation of similar responses in these peripheral cells. This results in the formation of wound-activated surface potential changes (WASPs). Additionally, Ca²⁺ regulates the expression of relevant genes through CaBP. Cell wall damage induces the production of OGs through the action of PG, which in turn regulates the expression of related genes through the MAPK pathway. This regulation impacts defense mechanisms, specifically the synthesis of JA, the generation of ROS signals, and callose production. The MAPK pathway also regulates HMG as cellular content, although the receptor remains unidentified.