Evidence map›Paper›PMID 32265497›Full record

ArticleCommunications biology2020

Trehalose metabolism confers developmental robustness and stability in Drosophila by regulating glucose homeostasis.

Ryota Matsushita, Takashi Nishimura

Open access · goldAbstract read
In one paragraph

Article in Communications biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
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

22 citing papers in PubMed, 52 citations in OpenAlex.

  1. Article
  2. Article
  3. Evolutionary Analysis of Trehalose Breakdown Pathways.Genome biology and evolution · 2026
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  20. Mild Muscle Mitochondrial Fusion Distress ExtendsInternational journal of molecular sciences · 2021
    Article
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 at 2 institutions in 1 country.

Ryota MatsushitaLaboratory for Growth Control Signaling, RIKEN Center for Biosystems Dynamics Research (BDR), 2-2-3 Minatojima-Minamimachi, Chuo-ku, Kobe, Hyogo, 650-0047, Japan.
Takashi NishimuraLaboratory for Growth Control Signaling, RIKEN Center for Biosystems Dynamics Research (BDR), 2-2-3 Minatojima-Minamimachi, Chuo-ku, Kobe, Hyogo, 650-0047, Japan. takashi.nishimura@riken.jp.
Nara Institute of Science and Technology · JPRIKEN Center for Biosystems Dynamics Research · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Organisms have evolved molecular mechanisms to ensure consistent and invariant phenotypes in the face of environmental fluctuations. Developmental homeostasis is determined by two factors: robustness, which buffers against environmental variations; and developmental stability, which buffers against intrinsic random variations. However, our understanding of these noise-buffering mechanisms remains incomplete. Here, we showed that appropriate glycemic control confers developmental homeostasis in the fruit fly Drosophila. We found that circulating glucose levels are buffered by trehalose metabolism, which acts as a glucose sink in circulation. Furthermore, mutations in trehalose synthesis enzyme (Tps1) increased the among-individual and within-individual variations in wing size. Whereas wild-type flies were largely resistant to changes in dietary carbohydrate and protein levels, Tps1 mutants experienced significant disruptions in developmental homeostasis in response to dietary stress. These results demonstrate that glucose homeostasis against dietary stress is crucial for developmental homeostasis.

Indexed as

Stress, PhysiologicalAnimal Nutritional Physiological PhenomenaAnimalsBlood GlucoseDietary CarbohydratesDrosophila melanogasterDrosophila ProteinsFemaleGenotypeGlucosyltransferasesHomeostasisMaleMutationNutritional StatusPhenotypeTrehaloseBlood GlucoseDietary CarbohydratesDrosophila ProteinsGlucosyltransferasesTrehalosetrehalose-6-phosphate synthase

Identifiers

PMID32265497
PMCPMC7138798
OpenAlexW3014603462

What OpenQuestion holds

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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.