School of Life and Environmental Sciences, The University of Sydney, Sydney, NSW, 2006, Australia.
Sci Rep. 2019 Jun 3;9(1):8216. doi: 10.1038/s41598-019-44726-x.
Regulatory mechanisms underlying thermal plasticity determine its evolution and potential to confer resilience to climate change. Here we show that class I and II histone deacetylases (HDAC) mediated thermal plasticity globally by shifting metabolomic profiles of cold acclimated zebrafish (Danio rerio) away from warm acclimated animals. HDAC activity promoted swimming performance, but reduced slow and fast myosin heavy chain content in cardiac and skeletal muscle. HDAC increased sarco-endoplasmic reticulum ATPase activity in cold-acclimated fish but not in warm-acclimated animals, and it promoted cardiac function (heart rate and relative stroke volume) in cold but not in warm-acclimated animals. HDAC are an evolutionarily ancient group of proteins, and our data show that they mediate the capacity for thermal plasticity, although the actual manifestation of plasticity is likely to be determined by interactions with other regulators such as AMP-activated protein kinase and thyroid hormone.
热塑性的调控机制决定了其进化和对气候变化的适应潜力。在这里，我们发现 I 类和 II 类组蛋白去乙酰化酶（HDAC）通过改变斑马鱼（Danio rerio）冷适应代谢组图谱，使其远离热适应动物，从而在全球范围内实现了热塑性。HDAC 活性促进了游泳性能，但减少了心脏和骨骼肌中慢肌和快肌肌球蛋白重链的含量。HDAC 增加了冷适应鱼类的肌浆内质网 ATP 酶活性，但在热适应动物中没有增加，并且促进了冷适应动物的心脏功能（心率和相对每搏输出量），但没有促进热适应动物的心脏功能。HDAC 是一组古老的蛋白质，我们的数据表明它们介导了热塑性的能力，尽管可塑性的实际表现可能取决于与其他调节剂（如 AMP 激活蛋白激酶和甲状腺激素）的相互作用。
