State Key Laboratory of Marine Environmental Science, College of Ocean and Earth Sciences, Xiamen University, Xiamen 361102, China.
Institute of Animal Genetic Resource, Nanjing Normal University, Nanjing 210046, China.
J Exp Biol. 2021 Oct 1;224(19). doi: 10.1242/jeb.243031. Epub 2021 Oct 5.
Thermal plasticity on different time scales, including acclimation/acclimatization and heat-hardening response - a rapid adjustment for thermal tolerance after non-lethal thermal stress, can interact to improve the resilience of organisms to thermal stress. However, little is known about physiological mechanisms mediating this interaction. To investigate the underpinnings of heat-hardening responses after acclimatization in warm seasons, we measured thermal tolerance plasticity, and compared transcriptomic and metabolomic changes after heat hardening at 33 or 37°C followed by recovery of 3 or 24 h in an intertidal bivalve Sinonovacula constricta. Clams showed explicit heat-hardening responses after acclimatization in a warm season. The higher inducing temperature (37°C) caused less effective heat-hardening effects than the inducing temperature that was closer to the seasonal maximum temperature (33°C). Metabolomic analysis highlighted the elevated content of glycerophospholipids in all heat-hardened clams, which may help to maintain the structure and function of the membrane. Heat shock proteins (HSPs) tended to be upregulated after heat hardening at 37°C but not at 33°C, indicating that there was no complete dependency of heat-hardening effects on upregulated HSPs. Enhanced energy metabolism and decreased energy reserves were observed after heat hardening at 37°C, suggesting more energy costs during exposure to a higher inducing temperature, which may restrict heat-hardening effects. These results highlight the mediating role of membrane lipid metabolism, heat shock responses and energy costs in the interaction between heat-hardening response and seasonal acclimatization, and contribute to the mechanistic understanding of evolutionary change and thermal plasticity during global climate change.
在不同时间尺度上的热塑性，包括驯化/适应和热硬化反应——在非致死热胁迫后对热耐受性的快速调整，可以相互作用提高生物体对热胁迫的恢复力。然而，对于介导这种相互作用的生理机制知之甚少。为了研究温暖季节驯化后热硬化反应的基础，我们测量了热耐受性可塑性，并比较了在 33 或 37°C 下进行热硬化后 3 或 24 小时恢复期间，在潮间带双壳类动物西施舌中的转录组和代谢组变化。在温暖季节驯化后，蛤蜊表现出明显的热硬化反应。较高的诱导温度（37°C）比接近季节性最高温度（33°C）的诱导温度产生的热硬化效果差。代谢组分析突出了所有热硬化蛤蜊中甘油磷脂含量的升高，这有助于维持膜的结构和功能。热休克蛋白（HSPs）在 37°C 下热硬化后趋于上调，但在 33°C 下则不然，这表明热硬化效果不完全依赖于 HSPs 的上调。在 37°C 下热硬化后观察到增强的能量代谢和减少的能量储备，表明在更高的诱导温度下暴露时需要更多的能量成本，这可能限制了热硬化效果。这些结果突出了膜脂代谢、热休克反应和能量成本在热硬化反应与季节性驯化之间相互作用中的介导作用，并有助于理解全球气候变化期间进化变化和热塑性的机制。
