ArticleEMBO reports2026
Notch-hedgehog antagonism regulates stem cell niche formation through an E2-E3-E3 ubiquitin module.
Article in EMBO reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
Abstract
Distinct microenvironments, including the stem cell niche and differentiation zone, promote stem cell self-renewal and progeny differentiation, yet how these domains are established remains unclear. In the developing Drosophila ovary, we show that Notch activation silences Hedgehog (Hh) signaling in anterior intermingled cells (ICs), specifying cap cells (CpCs) that form the germline stem cell (GSC) niche. Notch upregulates the E2 enzyme Ubc10, which partners with the RBR E3 ligase Ari-1 and a Cullin 3 (Cul3)-based RING E3 ligase to assemble an E2-E3-E3 complex, targeting Ci for degradation. By contrast, ICs posterior to CpCs retain Hh signaling and give rise to escort cells, forming the GSC differentiation zone. ARIH1, CUL3, and GLI2, the human orthologs of Ari-1, Cul3, and Ci, associate in human cells, suggesting conservation of this ubiquitin ligase module. Together, these findings identify a Notch-dependent E2-E3-E3 ubiquitin ligase module linking Notch activation to Hh silencing during niche patterning. This strategy may act broadly in cell-fate decisions and reveals a paradigm in which a developmental cue regulates an E2 enzyme to facilitate ubiquitin ligase assembly.
Identifiers
42850412What Socratic holds
Registered trials
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 Socratic graph.