Hu Shanming, Wang Yanan, Zhou Yongzhi, Cao Jie, Zhang Houshuang, Zhou Jinlin
Key Laboratory of Animal Parasitology of Ministry of Agriculture, Shanghai Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Shanghai, 200241, China.
Parasit Vectors. 2025 May 23;18(1):187. doi: 10.1186/s13071-025-06842-8.
The salivary glands of female ticks rapidly degenerate after feeding via programmed cell death mediated by an ecdysteroid receptor (ECR). The degeneration includes both apoptosis and autophagy. The process of degeneration can also be regulated by microRNAs (miRNAs), but the underlying mechanism of miRNA involvement in salivary gland degeneration remains incompletely understood. Here, we demonstrate that microRNA34-5p (miR-34-5p) regulates the process of salivary gland degeneration in Rhipicephalus haemaphysaloides by modulating the target gene RhECR.
Dual luciferase reporter assays and phenotypic rescue experiments identified RhECR as a direct target of miR-34-5p. The overexpression and inhibition of miR-34-5p were quantified by hematoxylin and eosin (H&E) and Terminal deoxynucleotidyl transferase dUTP Nick-End Labeling (TUNEL) staining.
The results showed that miR-34-5p inhibited the expression of RhECR to retard apoptosis in salivary gland acini. The study identified the roles of miR-34-5p and RhECR and their interactions in tick salivary gland degeneration.
The findings will aid in the application of ECR genes for tick control.
雌性蜱虫的唾液腺在通过蜕皮甾体受体（ECR）介导的程序性细胞死亡进食后迅速退化。这种退化包括细胞凋亡和自噬。退化过程也可由微小RNA（miRNA）调控，但miRNA参与唾液腺退化的潜在机制仍不完全清楚。在此，我们证明微小RNA34-5p（miR-34-5p）通过调节靶基因RhECR来调控血红扇头蜱唾液腺退化过程。
双荧光素酶报告基因检测和表型拯救实验确定RhECR是miR-34-5p的直接靶标。通过苏木精和伊红（H&E）染色以及末端脱氧核苷酸转移酶dUTP缺口末端标记（TUNEL）染色对miR-34-5p的过表达和抑制进行定量分析。
结果表明，miR-34-5p抑制RhECR的表达，从而延缓唾液腺腺泡中的细胞凋亡。该研究确定了miR-34-5p和RhECR在蜱唾液腺退化中的作用及其相互作用。
这些发现将有助于ECR基因在蜱虫控制中的应用。
