Evidence map›Paper›PMID 38885804›Full record

ArticleDevelopmental biology2024

Par3/bazooka binds NICD and promotes notch signaling during Drosophila development.

Jun Wu, Neeta Bala Tannan, Linh T Vuong, Yildiz Koca, Giovanna M Collu, Marek Mlodzik

Abstract read
In one paragraph

Article in Developmental biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. Review
  3. 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

6 authors.

Jun WuDept. of Cell, Developmental, and Regenerative Biology, Graduate School of Biomedical Sciences, Icahn School of Medicine at Mount Sinai, One Gustave L. Levy Place, New York, NY, 10029, USA.
Neeta Bala TannanDept. of Cell, Developmental, and Regenerative Biology, Graduate School of Biomedical Sciences, Icahn School of Medicine at Mount Sinai, One Gustave L. Levy Place, New York, NY, 10029, USA.
Linh T VuongDept. of Cell, Developmental, and Regenerative Biology, Graduate School of Biomedical Sciences, Icahn School of Medicine at Mount Sinai, One Gustave L. Levy Place, New York, NY, 10029, USA.
Yildiz KocaDept. of Cell, Developmental, and Regenerative Biology, Graduate School of Biomedical Sciences, Icahn School of Medicine at Mount Sinai, One Gustave L. Levy Place, New York, NY, 10029, USA.
Giovanna M ColluDept. of Cell, Developmental, and Regenerative Biology, Graduate School of Biomedical Sciences, Icahn School of Medicine at Mount Sinai, One Gustave L. Levy Place, New York, NY, 10029, USA.
Marek MlodzikDept. of Cell, Developmental, and Regenerative Biology, Graduate School of Biomedical Sciences, Icahn School of Medicine at Mount Sinai, One Gustave L. Levy Place, New York, NY, 10029, USA. Electronic address: marek.mlodzik@mssm.edu.

Funding

THE TISCH CANCER INSTITUTE - CANCER CENTER SUPPORT GRANTP30CA196521 · NCI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI Ramon E Parsons · 2015 to 2026
$35.4M
Retinal Patterning During Eye DevelopmentR01EY013256 · NEI · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI Marek Mlodzik · 2001 to 2026
$10.0M
Wnt/Frizzled-PCP signaling in development and diseaseR35GM127103 · NIGMS · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI Marek Mlodzik · 2018 to 2026
$5.6M
NCI NIH HHS P30 CA196521NEI NIH HHS R01 EY013256NIGMS NIH HHS R35 GM127103
6 · The paper itself

Abstract

The conserved bazooka (baz/par3) gene acts as a key regulator of asymmetrical cell divisions across the animal kingdom. Associated Par3/Baz-Par6-aPKC protein complexes are also well known for their role in the establishment of apical/basal cell polarity in epithelial cells. Here we define a novel, positive function of Baz/Par3 in the Notch pathway. Using Drosophila wing and eye development, we demonstrate that Baz is required for Notch signaling activity and optimal transcriptional activation of Notch target genes. Baz appears to act independently of aPKC in these contexts, as knockdown of aPKC does not cause Notch loss-of-function phenotypes. Using transgenic Notch constructs, our data positions Baz activity downstream of activating Notch cleavage steps and upstream of Su(H)/CSL transcription factor complex activity on Notch target genes. We demonstrate a biochemical interaction between NICD and Baz, suggesting that Baz is required for NICD activity before NICD binds to Su(H). Taken together, our data define a novel role of the polarity protein Baz/Par3, as a positive and direct regulator of Notch signaling through its interaction with NICD.

Indexed as

Drosophila ProteinsReceptors, NotchSignal TransductionWings, AnimalAnimalsCell PolarityDrosophilaDrosophila melanogasterEyeGene Expression Regulation, DevelopmentalIntracellular Signaling Peptides and ProteinsProtein Bindingbaz protein, DrosophilaDrosophila ProteinsIntracellular Signaling Peptides and ProteinsN protein, DrosophilaReceptors, NotchCell polarityDrosophilaNotch signalingPar3Tissue patterningTranscriptional target regulation

Identifiers

PMID38885804
PMCPMC11287782

What Socratic holds

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Registered trials

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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.