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Membrane lipid metabolism, heat shock response, and energy costs mediate the interaction between acclimatization and heat hardening response

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Jul 12, 2021 version files 361.31 KB
Aug 11, 2021 version files 361.44 KB

Abstract

Thermal plasticity on different timescales, including acclimation/acclimatization and heat hardening response – a rapid adjustment for thermal tolerance after a nonlethal thermal stress, can interact on organisms to improve the resilience to thermal stress. However, little is known about the physiological mechanisms mediating this interaction. To investigate underpinnings of heat hardening responses after acclimatization in warm season, we measured thermal tolerance plasticity, compared transcriptomic and metabolomic changes after heat hardening at 33 or 37oC followed by recovery of 3 h or 24 h in an intertidal bivalve Sinonovacula constricta. The clams showed explicit heat hardening responses after acclimatization in warm season. The higher inducing temperature (37oC) caused a less effective heat hardening effect than the inducing temperature that was closer to seasonal maximum temperature (33oC). Metabolomic analysis highlighted the elevated contents of membrane glyceropholipids in all heat hardened clams, which may help to maintain structure and function of membrane. Heat shock proteins (HSPs) tended to be up-regulated after heat hardening at 37oC but not at 33oC, indicating that there was no complete dependency of heat hardening effects on up-regulated HSPs. Enhanced energy metabolism and decreased energy reserves were observed after heat hardening at 37oC, suggesting more energy costs during exposure to higher inducing temperature which may restrict heat hardening effects. These results highlighted the mediating role of membrane lipid metabolism, heat shock responses and energy costs in the interaction of heat hardening response and seasonal acclimatization, and benefit the mechanistic understanding of evolutionary change and thermal plasticity during global climate change.