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用 17β-雌二醇使斑点叉尾鮰雌性化涉及到一组特定基因的甲基化和表达,而与性别决定区无关。

Feminization of channel catfish with 17β-oestradiol involves methylation and expression of a specific set of genes independent of the sex determination region.

机构信息

School of Fisheries, Aquaculture and Aquatic Sciences, Auburn University, Auburn, AL, USA.

Fujian Key Laboratory of Genetics and Breeding of Marine Organisms, College of Ocean and Earth Sciences, Xiamen University, Xiamen, Fujian, China.

出版信息

Epigenetics. 2022 Dec;17(12):1820-1837. doi: 10.1080/15592294.2022.2086725. Epub 2022 Jun 15.

Abstract

Exogenous oestrogen 17β-oestradiol (E2) has been shown to effectively induce feminization in teleosts. However, the molecular mechanisms underlying the process remain unclear. Here, we determined global DNA methylation and gene expression profiles of channel catfish () during early sex differentiation after E2 treatment. Overall, the levels of global DNA methylation after E2 treatment were not significantly different from those of controls. However, a specific set of genes were differentially methylated, which included many sex differentiation-related pathways, such as MARK signalling, adrenergic signalling, Wnt signalling, GnRH signalling, ErbB signalling, and ECM-receptor interactions. Many genes involved in these pathways were also differentially expressed after E2 treatment. Specifically, E2 treatments resulted in upregulation of female-related genes and downregulation of male-related genes in genetic males during sex reversal. However, E2-induced sex reversal did not cause sex-specific changes in methylation profiles or gene expression within the sex determination region (SDR) on chromosome 4, suggesting that E2-induced sex reversal was a downstream process independent of the sex determination process that was regulated by sex-specific methylation within the SDR.

摘要

外源性雌激素 17β-雌二醇 (E2) 已被证明能有效地诱导鱼类雌性化。然而,这一过程的分子机制尚不清楚。在这里,我们在 E2 处理后早期性别分化期间确定了斑点叉尾鮰 () 的全基因组 DNA 甲基化和基因表达谱。总体而言,E2 处理后的全基因组 DNA 甲基化水平与对照组没有显著差异。然而,一组特定的基因表现出差异甲基化,其中包括许多与性别分化相关的途径,如 MARK 信号、肾上腺素能信号、Wnt 信号、GnRH 信号、ErbB 信号和 ECM-受体相互作用。这些途径中的许多基因在 E2 处理后也表现出差异表达。具体来说,E2 处理导致在性反转过程中雄性个体中的雌性相关基因上调和雄性相关基因下调。然而,E2 诱导的性反转并没有导致性别决定区域 (SDR) 上的甲基化图谱或基因表达出现性别特异性变化 4 号染色体,这表明 E2 诱导的性反转是一个独立于性别决定过程的下游过程,由 SDR 内的性别特异性甲基化调控。

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