Evidence map›Paper›PMID 31153832›Full record

ArticleDevelopmental biology2019

Blood feeding activates the vitellogenic stage of oogenesis in the mosquito Aedes aegypti through inhibition of glycogen synthase kinase 3 by the insulin and TOR pathways.

Luca Valzania, Melissa T Mattee, Michael R Strand, Mark R Brown

Open access · greenAbstract read
In one paragraph

Article in Developmental biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 10% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

50 citing papers in PubMed, 1 synthesis or guideline pooled it, 88 citations in OpenAlex.

  1. Pooled it
  2. Sexually Dimorphic Visual Processing in the Yellow-Fever Mosquito,bioRxiv : the preprint server for biology · 2026
    Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. TheFrontiers in cellular and infection microbiology · 2026
    Article
  10. Review
  11. Article
  12. Article
  13. Genomic and insulin-mediated control of metabolic homeostasis by the mosquito ecdysone-induced gene E93.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  14. Article
  15. Article
  16. Review
  17. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Luca ValzaniaDepartment of Entomology, University of Georgia, Athens, GA, 30602, USA.
Melissa T MatteeDepartment of Entomology, University of Georgia, Athens, GA, 30602, USA.
Michael R StrandDepartment of Entomology, University of Georgia, Athens, GA, 30602, USA.
Mark R BrownDepartment of Entomology, University of Georgia, Athens, GA, 30602, USA. Electronic address: mrbrown@uga.edu.
University of Georgia · US

Funding

ENDOCRINOLOGY OF MOSQUITO REPRODUCTIONR01AI033108 · NIAID · UNIVERSITY OF GEORGIA (UGA) · PI STRAND, MICHAEL · 1992 to 2024
$5.8M
NIAID NIH HHS R01 AI033108
6 · The paper itself

Abstract

Most mosquitoes, including Aedes aegypti, only produce eggs after blood feeding on a vertebrate host. Oogenesis in A. aegypti consists of a pre-vitellogenic stage before blood feeding and a vitellogenic stage after blood feeding. Primary egg chambers remain developmentally arrested during the pre-vitellogenic stage but complete oogenesis to form mature eggs during the vitellogenic stage. In contrast, the signaling factors that maintain primary egg chambers in pre-vitellogenic arrest or that activate vitellogenic growth are largely unclear. Prior studies showed that A. aegypti females release insulin-like peptide 3 (ILP3) and ovary ecdysteroidogenic hormone (OEH) from brain neurosecretory cells after blood feeding. Here, we report that primary egg chambers exit pre-vitellogenic arrest by 8 h post-blood meal as evidenced by proliferation of follicle cells, endoreplication of nurse cells, and formation of cytoophidia. Ex vivo assays showed that ILP3 and OEH stimulate primary egg chambers to exit pre-vitellogenic arrest in the presence of nutrients but not in their absence. Characterization of associated pathways indicated that activation of insulin/insulin growth factor signaling (IIS) by ILP3 or OEH inactivated glycogen synthase kinase 3 (GSK3) via phosphorylation by phosphorylated Akt. GSK3 inactivation correlated with accumulation of the basic helix-loop-helix transcription factor Max and primary egg chambers exiting pre-vitellogenic arrest. Direct inhibition of GSK3 by CHIR-99021 also stimulated Myc/Max accumulation and primary egg chambers exiting pre-vitellogenic arrest. Collectively, our results identify GSK3 as a key factor in regulating the pre- and vitellogenic stages of oogenesis in A. aegypti.

Indexed as

AedesAnimalsBloodEatingEcdysteroidsFemaleGlycogen Synthase Kinase 3Insect ProteinsInsulinOogenesisOvaryOvumPhosphorylationReceptor, InsulinSignal TransductionTOR Serine-Threonine KinasesEcdysteroidsGlycogen Synthase Kinase 3Insect ProteinsInsulinReceptor, InsulinTOR Serine-Threonine KinasesEggHematophagyHormoneInsectReproductionSignaling

Identifiers

PMID31153832
PMCPMC6717557
OpenAlexW2947194342

What OpenQuestion holds

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Registered trials

None linked

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 OpenQuestion graph.