BMC biology · 2026
Loss of vitellogenin receptor function results in yolk depletion, virome expansion, and reduced bacterial load within the oocytes of Rhodnius prolixus.
СтатьяНазвание и аннотация: Перевод в очереди
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Amorim Juliana, Pereira Jéssica, das Neves Matheus, Rios Thamara, Nogueira Cintia Lopes, Braz Valdir, Reis Leonan, Faria-Reis Allana, Walter-Nuno Ana Beatriz, Selim Lukas, Nunes Daiene, de J C Baptista Thalysson Vinícius, Atella Georgia C, Laport Marinella Silva, Bahia Ana C, Logullo Carlos, Oliveira Pedro L, Paiva-Silva Gabriela O, Gondim Katia C, Ramos Isabela
Аннотация
BACKGROUND: The vitellogenin receptor (VgR) mediates yolk protein uptake during follicle development and is essential for embryogenesis in oviparous species. Here, we characterize the single Rhodnius prolixus VgR isoform and uncover an unexpected role in microbial regulation within the reproductive system.
RESULTS: The receptor displays a conserved LDLR-like structure and is highly expressed in early oocytes. RNAi-mediated VgR silencing caused defective yolk granule biogenesis, leading to the accumulation of the main yolk protein precursors, Vg and RHBP, in the hemolymph, yet oviposition and fertilization proceeded normally. The resulting eggs were yolk-depleted and non-viable. Remarkably, VgR knockdown reduced bacterial 16S rRNA levels in oocytes while promoting the expansion of several members of the core virome, a phenotype not reproduced by Vg silencing. Neither purified Vg nor changes in immune (defensin) or RNA interference pathways explained the microbial shifts.
CONCLUSIONS: These findings indicate that VgR influences not only yolk endocytosis but is also associated with changes in microbial composition within developing oocytes. We propose that VgR may contribute to a functional link between yolk endocytic dynamics and microbial homeostasis, thereby affecting the balance of microbial components in the oocyte. This connection broadens the functional context of VgR and provides new insight into how vertical transmission processes may be shaped in this major Chagas disease vector.
RESULTS: The receptor displays a conserved LDLR-like structure and is highly expressed in early oocytes. RNAi-mediated VgR silencing caused defective yolk granule biogenesis, leading to the accumulation of the main yolk protein precursors, Vg and RHBP, in the hemolymph, yet oviposition and fertilization proceeded normally. The resulting eggs were yolk-depleted and non-viable. Remarkably, VgR knockdown reduced bacterial 16S rRNA levels in oocytes while promoting the expansion of several members of the core virome, a phenotype not reproduced by Vg silencing. Neither purified Vg nor changes in immune (defensin) or RNA interference pathways explained the microbial shifts.
CONCLUSIONS: These findings indicate that VgR influences not only yolk endocytosis but is also associated with changes in microbial composition within developing oocytes. We propose that VgR may contribute to a functional link between yolk endocytic dynamics and microbial homeostasis, thereby affecting the balance of microbial components in the oocyte. This connection broadens the functional context of VgR and provides new insight into how vertical transmission processes may be shaped in this major Chagas disease vector.