Histone deacetylase activity mediates thermal plasticity in zebrafish (Danio rerio)

Frank Seebacher,Alec I M Simmonds

doi:10.1038/s41598-019-44726-x

Abstract

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.

Highlights

Resilience of animals to environmental variation determines population persistence, in the current era of rapid climate change[1,2]
The 95% confidence intervals overlapped between warm-acclimated control and TSAtreated fish indicating that these groups are similar statistically (Fig. 1)
We have shown that histone deacetylases (HDAC) activity alters physiological phenotypes in a temperature-dependent manner

Summary

Introduction

Resilience of animals to environmental variation determines population persistence, in the current era of rapid climate change[1,2]. The AMPK-HDAC axis could mediate responses to cold exposure such as increased locomotor performance and cardiac function associated with thermal acclimation[28,29]. We further predicted that these changes are accompanied by an increase in myosin heavy chain content, and a shift from fast to slow myosin heavy chain (MHC) isoforms in skeletal and heart muscle[33,34] We tested these hypotheses by conducting a fully factorial experiment with acclimation temperature (three week acclimation to either 18 °C or 28 °C), acute test temperature (18 °C and 28 °C), and TSA treatment (control, DMSO only, TSA dissolved in DMSO) as factors

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