Evidence map›Paper›PMID 39208453›Full record

ArticleG3 (Bethesda, Md.)2024

Genetic characterization of candidate ecdysteroid kinases in Drosophila melanogaster.

Jack L Scanlan, Charles Robin

Abstract read
In one paragraph

Article in G3 (Bethesda, Md.), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

2 authors.

Jack L ScanlanSchool of BioSciences, The University of Melbourne, Parkville Campus, Melbourne, Victoria 3010, Australia.
Charles RobinSchool of BioSciences, The University of Melbourne, Parkville Campus, Melbourne, Victoria 3010, Australia.ORCID 0000-0002-7733-6763

Funding

Resource Project CoreU41HG000739 · NHGRI · HARVARD UNIVERSITY · PI PERRIMON, NORBERT · 2014 to 2022
$32.3M
Resource Component: Acquisition, maintenance and distribution of Drosophila stocksP40OD018537 · OD · TRUSTEES OF INDIANA UNIVERSITY · PI Annette L. Parks · 2014 to 2026
$13.5M
DROSOPHILA GENOMICS RESOURCE CENTERP40OD010949 · OD · TRUSTEES OF INDIANA UNIVERSITY · PI Andrew Zelhof · 2012 to 2026
$9.4M
Australian Government stipendNHGRI NIH HHS U41 HG000739NIH HHS P40 OD010949NIH HHS P40 OD018537University of Melbourne
6 · The paper itself

Abstract

Ecdysteroids are major hormones in insects and control molting, growth, reproduction, physiology, and behavior. The biosynthesis of ecdysteroids such as 20-hydroxyecdysone (20E) from dietary sterols is well characterized, but ecdysteroid catabolism is poorly understood. Ecdysteroid kinases (EcKs) mediate the reversible phosphorylation of ecdysteroids, which has been implicated in ecdysteroid recycling during embryogenesis and reproduction in various insects. However, to date, only 2 EcK-encoding genes have been identified, in the silkworm Bombyx mori and the mosquito Anopheles gambiae. Previously, we identified 2 ecdysteroid kinase-like (EcKL) genes-Wallflower (Wall) and Pinkman (pkm)-in the model fruit fly Drosophila melanogaster that are orthologs of the ecdysteroid 22-kinase gene BmEc22K. Here, using gene knockdown, knockout, and misexpression, we explore Wall and pkm's possible functions and genetically test the hypothesis that they encode EcKs. Wall and pkm null mutants are viable and fertile, suggesting that they are not essential for development or reproduction, whereas phenotypes arising from RNAi and somatic CRISPR appear to derive from off-target effects or other artifacts. However, misexpression of Wall results in dramatic phenotypes, including developmental arrest, and defects in trachea, cuticle, and pigmentation. Wall misexpression fails to phenocopy irreversible ecdysteroid catabolism through misexpression of Cyp18a1, suggesting that Wall does not directly inactivate 20E. Additionally, Wall misexpression phenotypes are not attenuated in Cyp18a1 mutants, strongly suggesting that Wall is not an ecdysteroid 26-kinase. We hypothesize that the substrate of Wall in this misexpression experiment and possibly generally is an unknown, atypical ecdysteroid that plays essential roles in Drosophila development, and may highlight aspects of insect endocrinology that are as-yet uncharacterized. We also provide preliminary evidence that CG5644 encodes an ecdysteroid 22-kinase conserved across Diptera.

Indexed as

Drosophila melanogasterEcdysteroidsAnimalsDrosophila ProteinsFemaleMutationPhenotypeDrosophila ProteinsEcdysteroids20-hydroxyecdysone3-dehydroecdysoneCRISPRecdysoneRNAisteroidtracheaUAS/GAL4

Identifiers

PMID39208453
PMCPMC12117438

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.