Elevated CO2 can protect plants from heat stress (HS); however, the underlying mechanisms are largely unknown. Here, we used a set of Arabidopsis mutants such as salicylic acid (SA) signaling mutants nonexpressor of pathogenesis-related gene 1 (npr1-1 and npr1-5) and heat-shock proteins (HSPs) mutants (hsp21 and hsp70-1) to understand the requirement of SA signaling and HSPs in elevated CO2-induced HS tolerance. Under ambient CO2 (380 µmol mol(-1)) conditions, HS (42°C, 24 h) drastically decreased maximum photochemical efficiency of PSII (Fv/Fm) in all studied plant groups. Enrichment of CO2 (800 µmol mol(-1)) with HS remarkably increased the Fv/Fm value in all plant groups except hsp70-1, indicating that NPR1-dependent SA signaling is not involved in the elevated CO2-induced HS tolerance. These results also suggest an essentiality of HSP70-1, but not HSP21 in elevated CO2-induced HS mitigation.
Keywords: ABA; Arabidopsis; PSII; photosystems II; SA; abscisic acid; Fv/Fm; elevated carbon dioxide; heat stress; heat stress; HSPs; heat-shock proteins; heat-shock proteins; MAPK; maximum photochemical efficiency of PSII; HS; mitogen activated protein kinase; npr1; nonexpressor of pathogenesis-related gene 1; photochemical efficiency of PSII; salicylic acid; salicylic acid..