Short photoperiod inhibited gonadal growth and elevated hypothalamic Dio3 expression unrelated to promoter DNA methylation in young Brandt's voles
文献类型: 外文期刊
第一作者: Qiao, Yanting
作者: Qiao, Yanting;Li, Ning;Song, Ying;Liu, Xiaohui;Wang, Dawei;Wang, Dawei;Wang, Dawei
作者机构:
关键词: Brandt's vole; Dio3; DNA methylation; seasonal breeding; shortening photoperiod
期刊名称:INTEGRATIVE ZOOLOGY ( 影响因子:3.5; 五年影响因子:3.0 )
ISSN: 1749-4877
年卷期: 2024 年
页码:
收录情况: SCI
摘要: Photoperiod, the length of daylight, has a significant impact on the physiological characteristics of seasonal breeding animals, including their somatic and gonadal development. In rodents, expression of deiodinase type II (Dio2) and III (Dio3) in the hypothalamus is crucial for responding to photoperiodic signals. However, research on the photoperiodism of hypothalamic gene expression and the corresponding regulatory mechanism in Brandt's voles living in the Mongolian steppes is limited. In this study, we gradually changed day length patterns to simulate spring (increasing long photoperiod, ILP) and autumn (decreasing short photoperiod, DSP). We compared the somatic and gonadal development of voles born under ILP and DSP and the expression patterns of five reproduction-related genes in the hypothalamus of young voles. The results showed that DSP significantly inhibited somatic and gonadal development in both female and male offspring. Compared with ILP, Dio3 expression was significantly upregulated in the hypothalamus under DSP conditions and remained elevated until postnatal week 8 in both males and females. However, there was no significant difference in the methylation levels of the proximal promoter region of Dio3 between ILP and DSP, suggesting that methylation in the proximal promoter region may not be involved in regulating the expression of Dio3. These findings suggest that hypothalamic expression of Dio3 plays a key role in the photoperiodic regulation of gonadal activity in Brandt's voles. However, it appears that CpGs methylation in the promoter region is not the main mechanism regulating Dio3 expression.
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