Aug 2026· Insect Biochemistry and Molecular Biology· pp.
104664
· 0 citations· 64 references
Medicine
TL;DR
DmaxVgR gene silencing disrupted follicular architecture and reduced vitellogenin uptake by the oocytes, resulting in increased vitellogenin levels in the hemolymph suggest a feedback mechanism regulating YPP production.
Abstract
Reproduction in insects is a tightly regulated process that relies on the accumulation of yolk protein precursors (YPPs) to support embryonic development. Vitellogenin, the main YPP, is synthesized in the fat body-analogous to the liver and adipose tissue of vertebrates-and transported through the hemolymph to the ovarian follicles, where it is internalized by developing oocytes via the vitellogenin receptor (VgR). Despite its essential role in vitellogenesis, the functional characterization of insect VgR remains incomplete. Triatomines are hematophagous insects and vectors of Trypanosoma cruzi, the causative agent of Chagas disease. In this study, we characterized the VgR of Dipetalogaster maxima (DmaxVgR), a triatomine species, using biochemical, molecular, and bioinformatics approaches. The DmaxVgR gene was cloned, sequenced, and annotated, revealing a highly conserved protein sequence. Phylogenetic analysis clustered VgR amino acid sequences by taxonomic groups. Structural modeling of DmaxVgR showed a conserved folding pattern, enabling docking analyses with a modeled vitellogenin and indicating a stable interaction between the two proteins. DmaxVgR gene silencing disrupted follicular architecture and reduced vitellogenin uptake by the oocytes, resulting in increased vitellogenin levels in the hemolymph. Concurrently, elevated vitellogenin transcript levels and vitellogenin amounts in the fat body suggest a feedback mechanism regulating YPP production. Together, our findings provide new insights into the role and molecular regulation of VgR in triatomine reproduction and offer a framework for future studies exploring its potential relevance for vector control strategies.
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