Evidence map›Paper›PMID 30929905›Full record

ArticleCell2019

Steroid Hormone Function Controls Non-competitive Plasmodium Development in Anopheles.

Kristine Werling, W Robert Shaw, Maurice A Itoe, Kathleen A Westervelt, Perrine Marcenac, Douglas G Paton, Duo Peng, Naresh Singh, Andrea L Smidler, Adam South and 8 more

Abstract read
In one paragraph

Article in Cell, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
–field-weighted citation impact
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

62 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. PfApiAT2 is a proline transporter essential for the transmission ofbioRxiv : the preprint server for biology · 2026
    Article
  8. Article
  9. Article
  10. Article
  11. MappingbioRxiv : the preprint server for biology · 2025
    Article
  12. Article
  13. Review
  14. Article
  15. OocystMeter, a machine-learning algorithm to count and measurebioRxiv : the preprint server for biology · 2025
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

2 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

18 authors.

Kristine WerlingDepartment of Immunology and Infectious Diseases, Harvard T.H. Chan School of Public Health, Boston, MA 02115, USA.
W Robert ShawDepartment of Immunology and Infectious Diseases, Harvard T.H. Chan School of Public Health, Boston, MA 02115, USA.
Maurice A ItoeDepartment of Immunology and Infectious Diseases, Harvard T.H. Chan School of Public Health, Boston, MA 02115, USA.
Kathleen A WesterveltDepartment of Immunology and Infectious Diseases, Harvard T.H. Chan School of Public Health, Boston, MA 02115, USA.
Perrine MarcenacDepartment of Immunology and Infectious Diseases, Harvard T.H. Chan School of Public Health, Boston, MA 02115, USA.
Douglas G PatonDepartment of Immunology and Infectious Diseases, Harvard T.H. Chan School of Public Health, Boston, MA 02115, USA.
Duo PengDepartment of Immunology and Infectious Diseases, Harvard T.H. Chan School of Public Health, Boston, MA 02115, USA.
Naresh SinghDepartment of Immunology and Infectious Diseases, Harvard T.H. Chan School of Public Health, Boston, MA 02115, USA.
Andrea L SmidlerDepartment of Immunology and Infectious Diseases, Harvard T.H. Chan School of Public Health, Boston, MA 02115, USA; Wyss Institute for Biologically Inspired Engineering, Boston, MA 02115, USA.
Adam SouthDepartment of Immunology and Infectious Diseases, Harvard T.H. Chan School of Public Health, Boston, MA 02115, USA.
Amy A DeikBroad Institute, Cambridge, MA 02142, USA.
Liliana Mancio-SilvaInstitute for Medical Engineering and Science, Massachusetts Institute of Technology, Cambridge, MA 02142, USA.
Allison R DemasInstitute for Medical Engineering and Science, Massachusetts Institute of Technology, Cambridge, MA 02142, USA.
Sandra MarchInstitute for Medical Engineering and Science, Massachusetts Institute of Technology, Cambridge, MA 02142, USA.
Eric CalvoLaboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, NIH, Rockville, MD 20852, USA.
Sangeeta N BhatiaBroad Institute, Cambridge, MA 02142, USA; Institute for Medical Engineering and Science, Massachusetts Institute of Technology, Cambridge, MA 02142, USA; Howard Hughes Medical Institute, Chevy Chase, MD 20815, USA; Koch Institute for Integrative Cancer Research, Cambridge, MA 02142, USA; Department of Medicine, Brigham and Women's Hospital, Boston, MA 02115, USA.
Clary B ClishBroad Institute, Cambridge, MA 02142, USA.
Flaminia CatterucciaDepartment of Immunology and Infectious Diseases, Harvard T.H. Chan School of Public Health, Boston, MA 02115, USA. Electronic address: fcatter@hsph.harvard.edu.

Funding

Arthropod saliva in vector-borne disease transmission: Functional analysis of novel domains in salivary secretionsZIAAI001246 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI CALVO, ERIC · 2019 to 2025
$10.0M
Targeting steroid hormone signaling in Anopheles mosquitoes for malaria controlR01AI124165 · NIAID · HARVARD SCHOOL OF PUBLIC HEALTH · PI CATTERUCCIA, FLAMINIA · 2016 to 2020
$3.4M
Targeting the reproductive interactome of the malaria vector Anopheles gambiaeR01AI104956 · NIAID · HARVARD SCHOOL OF PUBLIC HEALTH · PI CATTERUCCIA, FLAMINIA · 2013 to 2017
$3.0M
Using genome engineering to study mosquito biology and combat malariaF31AI120480 · NIAID · HARVARD SCHOOL OF PUBLIC HEALTH · PI SMIDLER, ANDREA LYNELLE · 2016 to 2018
$74k
Howard Hughes Medical InstituteNIAID NIH HHS F31 AI120480NIAID NIH HHS R01 AI104956NIAID NIH HHS R01 AI124165
6 · The paper itself

Abstract

Transmission of malaria parasites occurs when a female Anopheles mosquito feeds on an infected host to acquire nutrients for egg development. How parasites are affected by oogenetic processes, principally orchestrated by the steroid hormone 20-hydroxyecdysone (20E), remains largely unknown. Here we show that Plasmodium falciparum development is intimately but not competitively linked to processes shaping Anopheles gambiae reproduction. We unveil a 20E-mediated positive correlation between egg and oocyst numbers; impairing oogenesis by multiple 20E manipulations decreases parasite intensities. These manipulations, however, accelerate Plasmodium growth rates, allowing sporozoites to become infectious sooner. Parasites exploit mosquito lipids for faster growth, but they do so without further affecting egg development. These results suggest that P. falciparum has adopted a non-competitive evolutionary strategy of resource exploitation to optimize transmission while minimizing fitness costs to its mosquito vector. Our findings have profound implications for currently proposed control strategies aimed at suppressing mosquito populations.

Indexed as

AnimalsAnophelesCulicidaeEcdysteroneFemaleHEK293 CellsHost-Parasite InteractionsHumansInsect VectorsMalariaMalaria, FalciparumMiceMosquito VectorsNIH 3T3 CellsOogenesisPlasmodiumEcdysteroneSteroids20E signalingAnopheles-Plasmodium interactionsEIPextrinsic incubation periodlipid transporttrade-offs

Identifiers

PMID30929905
PMCPMC6450776

What OpenQuestion holds

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Read underepoch 390

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.