AbstractPrevious physiological and pharmacological studies have suggested that the activity of phosphoinositide‐specific phospholipase C (PI‐PLC) plays an important role in regulating plant salt stress responses by altering the intracellular Ca2+ concentration. However, the individual members of plant PLCs involved in this process need to be identified. Here, the function of AtPLC4 in the salt stress response of Arabidopsis seedlings was analysed. plc4 mutant seedlings showed hyposensitivity to salt stress compared with Col‐0 wild‐type seedlings, and the salt hyposensitive phenotype could be complemented by the expression of native promoter‐controlled AtPLC4. Transgenic seedlings with AtPLC4 overexpression (AtPLC4 OE) exhibited a salt‐hypersensitive phenotype, while transgenic seedlings with its inactive mutant expression (AtPLC4m OE) did not exhibit this phenotype. Using aequorin as a Ca2+ indicator in plc4 mutant and AtPLC4 OE seedlings, AtPLC4 was shown to positively regulate the salt‐induced Ca2+ increase. The salt‐hypersensitive phenotype of AtPLC4 OE seedlings was partially rescued by EGTA. An analysis of salt‐responsive genes revealed that the transcription of RD29B, MYB15 and ZAT10 was inversely regulated in plc4 mutant and AtPLC4 OE seedlings. Our findings suggest that AtPLC4 negatively regulates the salt tolerance of Arabidopsis seedlings, and Ca2+ may be involved in regulating this process.