Fig. 2

Wounding induces Ca²⁺ and mitochondrial responses that promote actin-polymerization to repair the wound. Wounding can trigger an instant rise in the epidermal cytosolic Ca²⁺ level. TRPM channel GTL-2 in the plasma membrane and IP3 receptor ITR-1 located at the endoplasmic reticulum contributes to the initial of Ca²⁺ activation. Through the mitochondrial Ca²⁺ uniporter MCU-1, cytosolic Ca²⁺ enters into the mitochondria matrix and triggers the production of mtROS. Besides, Ca²⁺ also regulates wound-induced mitochondrial fragmentation (WIMF) through the outer mitochondrial membrane protein MIRO-1 to enhance the mtROS signals. The epidermal wound is essentially closed by direct actin polymerization, which is dependent on Ca²⁺ activation. mtROS regulates the local activation of small GTPases RHO-1 to promote actin polymerization based wound closure