Department of Biology and Institute of Biochemistry, Carleton University, 1125 Colonel By Drive, Ottawa, ON, K1S 5B6, Canada.
Mar Biotechnol (NY). 2024 Nov 22;27(1):5. doi: 10.1007/s10126-024-10394-w.
Northern Crayfish, Faxonius virilis, displays various strategies that allow them to survive extended periods of oxygen deprivation. However, certain epigenetic adaptations that these crayfish use have not been studied in detail, and the role of specific mechanisms used such as histone modifications remain unknown. Epigenetic studies offer a new perspective on how crayfish can regulate gene expression to redirect energy to essential functions needed for survival. This study investigates the regulation of histone modifications of proteins including acetylation and deacetylation in F. virilis in response to 20-h anoxia exposure. These histone modifications were studied via analysis of writer, reader, and eraser proteins such as lysine acetyltransferases (KATs), bromodomain proteins (BRDs), histone deacetylases (HDAC), and sirtuin proteins (SIRTs). Significant upregulation was seen in one histone protein and one lysine acetyltransferase: H3K14Ac and KAT2A. These proteins are known to be regulated by BRD2; a protein that specifically reads and targets H3K14Ac. In response to anoxia, a larger number of histone deacetylases and sirtuin proteins were upregulated in comparison to lysine acetyltransferases suggesting a focus on suppression of gene expression. The histone deacetylases and sirtuin proteins with significant upregulation were HDAC2, HDAC3, SIRT2, SIRT3, and SIRT6. These proteins have also all been implicated in DNA damage regulation which further suggests that crayfish focus limited energy on ensuring cell survival. This study provides an understanding of how histone acetylation and deacetylation are regulated in crayfish as a component of metabolic rate suppression under anoxia.
北方淡水螯虾 Faxonius virilis 表现出多种策略，使它们能够在长时间缺氧的情况下存活。然而，这些螯虾使用的某些表观遗传适应机制尚未被详细研究，例如组蛋白修饰等特定机制的作用仍然未知。表观遗传学研究为螯虾如何调节基因表达提供了新的视角，使它们能够将能量重新分配到生存所需的基本功能上。本研究调查了在 20 小时缺氧暴露下，F. virilis 中组蛋白修饰蛋白（包括乙酰化和去乙酰化）的调节。通过分析赖氨酸乙酰转移酶（KATs）、溴结构域蛋白（BRDs）、组蛋白去乙酰化酶（HDACs）和 Sirtuin 蛋白（SIRTs）等写入器、读取器和擦除器蛋白来研究这些组蛋白修饰。一种组蛋白蛋白和一种赖氨酸乙酰转移酶 KAT2A 的表达显著上调。已知这些蛋白受 BRD2 调节，BRD2 是一种特异性读取和靶向 H3K14Ac 的蛋白。与赖氨酸乙酰转移酶相比，在缺氧应激下，更多的组蛋白去乙酰化酶和 Sirtuin 蛋白上调，表明它们更专注于抑制基因表达。表达显著上调的组蛋白去乙酰化酶和 Sirtuin 蛋白包括 HDAC2、HDAC3、SIRT2、SIRT3 和 SIRT6。这些蛋白也都与 DNA 损伤调节有关，这进一步表明螯虾将有限的能量集中在确保细胞存活上。本研究提供了对组蛋白乙酰化和去乙酰化在螯虾中的调节机制的理解，这是在缺氧条件下代谢率抑制的一个组成部分。
