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Background <p>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 <i>Rhipicephalus haemaphysaloides</i> by modulating the target gene RhECR. </p> Methods <p>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&amp;E) and Terminal deoxynucleotidyl transferase dUTP Nick-End Labeling (TUNEL) staining.</p> Results <p>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.</p> Conclusions <p>The findings will aid in the application of ECR genes for tick control.</p> Graphical Abstract <p></p>

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MicroRNA-34-5p regulates the expression of ecdysteroid receptor (ECR) in the process of salivary gland degeneration of ticks

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年5月23日

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  • Shanming Hu,
  • Yanan Wang,
  • Yongzhi Zhou,
  • Jie Cao,
  • Houshuang Zhang,
  • Jinlin Zhou

摘要

Background

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.

Methods

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.

Results

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.

Conclusions

The findings will aid in the application of ECR genes for tick control.

Graphical Abstract