Evidence map›Paper›PMID 35112131›Full record

ArticleDevelopment (Cambridge, England)2022

Notch signaling regulates neural stem cell quiescence entry and exit in Drosophila.

Chhavi Sood, Virginia T Justis, Susan E Doyle, Sarah E Siegrist

Open access · bronzeAbstract read
In one paragraph

Article in Development (Cambridge, England), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

17 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Temporal Transcriptional Regulation of Human Neuronal Differentiation via Forward Programming.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  7. Review
  8. Article
  9. Article
  10. Modes of Notch signalling in development and disease.Nature reviews. Molecular cell biology · 2025
    Review
  11. Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
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.

Chhavi SoodDepartment of Biology, University of Virginia, Charlottesville, VA 22904, USA.ORCID 0000-0002-3813-5774
Virginia T JustisDepartment of Biology, University of Virginia, Charlottesville, VA 22904, USA.
Susan E DoyleDepartment of Biology, University of Virginia, Charlottesville, VA 22904, USA.
Sarah E SiegristDepartment of Biology, University of Virginia, Charlottesville, VA 22904, USA.ORCID 0000-0003-0685-5387
University of Virginia · US

Funding

Nutrient-dependent regulation of neural stem cell proliferation and neural circuit formationR35GM141886 · NIGMS · UNIVERSITY OF VIRGINIA · PI SIEGRIST, SARAH ELIZABETH · 2021 to 2025
$2.3M
Cell growth and proliferation control in neural stem cellsR01GM120421 · NIGMS · UNIVERSITY OF VIRGINIA · PI SIEGRIST, SARAH ELIZABETH · 2016 to 2020
$1.6M
NIGMS NIH HHS R01 GM120421NIGMS NIH HHS R35 GM141886
6 · The paper itself

Abstract

Stem cells enter and exit quiescence as part of normal developmental programs and to maintain tissue homeostasis in adulthood. Although it is clear that stem cell intrinsic and extrinsic cues, local and systemic, regulate quiescence, it remains unclear whether intrinsic and extrinsic cues coordinate to control quiescence and how cue coordination is achieved. Here, we report that Notch signaling coordinates neuroblast intrinsic temporal programs with extrinsic nutrient cues to regulate quiescence in Drosophila. When Notch activity is reduced, quiescence is delayed or altogether bypassed, with some neuroblasts dividing continuously during the embryonic-to-larval transition. During embryogenesis before quiescence, neuroblasts express Notch and the Notch ligand Delta. After division, Delta is partitioned to adjacent GMC daughters where it transactivates Notch in neuroblasts. Over time, in response to intrinsic temporal cues and increasing numbers of Delta-expressing daughters, neuroblast Notch activity increases, leading to cell cycle exit and consequently, attenuation of Notch pathway activity. Quiescent neuroblasts have low to no active Notch, which is required for exit from quiescence in response to nutrient cues. Thus, Notch signaling coordinates proliferation versus quiescence decisions.

Indexed as

Signal TransductionAnimalsCell CycleDrosophilaDrosophila ProteinsEmbryonic DevelopmentEmbryo, NonmammalianHippo KinasesIntracellular Signaling Peptides and ProteinsNeural Stem CellsNeuronsNuclear ProteinsProtein Serine-Threonine KinasesReceptors, Notchdap protein, DrosophilaDrosophila ProteinsHippo Kinaseshpo protein, DrosophilaIntracellular Signaling Peptides and ProteinsNuclear ProteinsProtein Serine-Threonine KinasesReceptors, NotchAsymmetric cell divisionCell cycleDacapoDeltaDrosophilaHippoNeural stem cellNeuroblastNotch signalingPI3-kinaseQuiescenceTribbles

Identifiers

PMID35112131
PMCPMC8918809
OpenAlexW4210757750

What OpenQuestion holds

Textmetadata
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.