[Ca2+]cyt response to elicitor, cold, and heat in the aca8 aca10 mutant. [Ca2+]cyt responses to flg22 A), cold B), and heat C) in epidermal cells of wild-type Col-0 and aca8 aca10 fmo1 mutant measured by the mCherry-GCaMP6f reporter. Shown are averages and SD (error bars) of the GFP/RFP ratio (upper panel) and fractional ratio changes ΔR/R0 (lower panel). In A), signals in response to 200 nM flg22 were captured every minute, and signals from 15 min before the peak to 20 min after the peak from a total of 8 cells (1 cell/plant) for each genotype are aligned at the peak. For B), leaves were taped on slides, and ice water was added to a slide as cold treatment. Arrow indicates the time of cold application. Data were from a total of 12 cells (1 cell/plant) for each genotype. For C), leaves were taped on slides, and heat treatment was applied by adding water of 42 °C to slides. Arrow indicates the time of heat application. Data are from 10 cells (1 cell/plant) for each genotype. D) Model of calmodulin-regulated Ca2+ pumps function. The primary functions of PM-localized Ca2+ pumps ACA8 and ACA10 as well as the vacuole-localized pumps ACA4 and ACA11 are to maintain low resting [Ca2+]cyt, and the resting level of [Ca2+]cyt has a large impact on biotic and abiotic stress responses. Elevated resting [Ca2+]cyt in the aca8 aca10 or aca4 aca11 mutants causes autoimmunity with mis-regulated expression of defense response genes. Under chilling, this autoimmunity is amplified leading to cell death and chilling susceptibility. Under heat, elevated resting [Ca2+]cyt induces closed stomata and heat susceptibility.