ArticleBMC biology2026
Loss of vitellogenin receptor function results in yolk depletion, virome expansion, and reduced bacterial load within the oocytes of Rhodnius prolixus.
Article in BMC biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
20 authors.
Funding
Abstract
backgroundThe 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.
resultsThe 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.
conclusionsThese 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.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.