Ca2+ influences heat shock signal transduction in Pyropia haitanensis

Recently, high-temperature stress induced by climate change has resulted in the degradation of Pyropia haitanensis thalli, which has adversely affected the P. haitanensis aquaculture industry. Although heat-resistant P. haitanensis strains have been developed, the mechanism underlying the stress resistance remains unclear. In this study, we investigated the effects of high-temperature stress (32 °C) on the Ca2+ flux and calmodulin (CaM) contents of P. haitanensis thalli. Gene expression and protein abundance were also analyzed. The high-temperature stress significantly increased the Ca2+ influx, as well as the expression levels of CaMs and their encoded proteins. However, when the plasma membrane Ca2+ channel was inhibited by verapamil, the Ca2+ influx, CaM expression levels, CaM abundance levels, and photosynthetic activities decreased considerably. These changes ultimately reduced the heat resistance of P. haitanensis thalli. Additionally, the expression levels of heat shock protein genes (HSP22 and HSP70) were upregulated under high-temperature conditions, whereas they were downregulated after the Ca2+ influx rate decreased. Thus, the Ca2+ signal generated by the plasma membrane's Ca2+ channels appears to be important for P. haitanensis responses to high-temperature stress. The data presented herein provide insights into the mechanisms responsible for P. haitanensis' heat resistance. •High-temperature stress induces considerable Ca2+ influx within 15 min of treatment.•Ca2+ and calmodulin mediate responses to high-temperature stress in P. haitanensis.•Ca2+ and calmodulin may regulate HSP expression levels.