Evidence map›Paper›PMID 36413949›Full record

ArticleDevelopmental cell2022

Neuronal-epithelial cross-talk drives acinar specification via NRG1-ERBB3-mTORC2 signaling.

Alison J May, Aaron J Mattingly, Eliza A Gaylord, Nathan Griffin, Sonia Sudiwala, Noel Cruz-Pacheco, Elaine Emmerson, Seayar Mohabbat, Sara Nathan, Hanan Sinada and 2 more

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Developmental cell, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.7field-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

13 citing papers in PubMed, 17 citations in OpenAlex.

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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

12 authors at 2 institutions in 1 country.

Alison J MayProgram in Craniofacial Biology, University of California, 513 Parnassus Avenue, San Francisco, CA 94143, USA; Department of Cell and Tissue Biology, University of California, 513 Parnassus Avenue, San Francisco, CA 94143, USA.
Aaron J MattinglyProgram in Craniofacial Biology, University of California, 513 Parnassus Avenue, San Francisco, CA 94143, USA; Department of Cell and Tissue Biology, University of California, 513 Parnassus Avenue, San Francisco, CA 94143, USA.
Eliza A GaylordProgram in Craniofacial Biology, University of California, 513 Parnassus Avenue, San Francisco, CA 94143, USA; Department of Cell and Tissue Biology, University of California, 513 Parnassus Avenue, San Francisco, CA 94143, USA.
Nathan GriffinProgram in Craniofacial Biology, University of California, 513 Parnassus Avenue, San Francisco, CA 94143, USA; Department of Cell and Tissue Biology, University of California, 513 Parnassus Avenue, San Francisco, CA 94143, USA.
Sonia SudiwalaProgram in Craniofacial Biology, University of California, 513 Parnassus Avenue, San Francisco, CA 94143, USA; Department of Cell and Tissue Biology, University of California, 513 Parnassus Avenue, San Francisco, CA 94143, USA.
Noel Cruz-PachecoProgram in Craniofacial Biology, University of California, 513 Parnassus Avenue, San Francisco, CA 94143, USA; Department of Cell and Tissue Biology, University of California, 513 Parnassus Avenue, San Francisco, CA 94143, USA.
Elaine EmmersonProgram in Craniofacial Biology, University of California, 513 Parnassus Avenue, San Francisco, CA 94143, USA; Department of Cell and Tissue Biology, University of California, 513 Parnassus Avenue, San Francisco, CA 94143, USA.
Seayar MohabbatProgram in Craniofacial Biology, University of California, 513 Parnassus Avenue, San Francisco, CA 94143, USA; Department of Cell and Tissue Biology, University of California, 513 Parnassus Avenue, San Francisco, CA 94143, USA.
Sara NathanProgram in Craniofacial Biology, University of California, 513 Parnassus Avenue, San Francisco, CA 94143, USA; Department of Cell and Tissue Biology, University of California, 513 Parnassus Avenue, San Francisco, CA 94143, USA.
Hanan SinadaProgram in Craniofacial Biology, University of California, 513 Parnassus Avenue, San Francisco, CA 94143, USA; Department of Cell and Tissue Biology, University of California, 513 Parnassus Avenue, San Francisco, CA 94143, USA.
Isabelle M A LombaertBiointerfaces Institute, University of Michigan, 2800 Plymouth Rd, Ann Arbor, MI 48109, USA; Department of Biologic and Materials Sciences & Prosthodontics, School of Dentistry, University of Michigan, 1011 N University Ave, Ann Arbor, MI 48109, USA. Electronic address: lombaert@umich.edu.
Sarah M KnoxProgram in Craniofacial Biology, University of California, 513 Parnassus Avenue, San Francisco, CA 94143, USA; Department of Cell and Tissue Biology, University of California, 513 Parnassus Avenue, San Francisco, CA 94143, USA. Electronic address: sarah.knox@ucsf.edu.
University of California, San Francisco · USUniversity of Michigan · US

Funding

Defining mechanisms driving salivary gland regenerationR35DE028255 · NIDCR · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI KNOX, SARAH MONICA · 2018 to 2025
$7.7M
Neuronal regulation of salivary stem cellsR01DE024188 · NIDCR · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI KNOX, SARAH MONICA · 2014 to 2018
$2.0M
Defining the role of ERBB3 in salivary acinar cell developmentF31DE027607 · NIDCR · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI MATTINGLY, AARON JOSHUA · 2017 to 2018
$75k
Medical Research Council MR/R015635/1NIDCR NIH HHS F31 DE027607NIDCR NIH HHS R01 DE024188NIDCR NIH HHS R35 DE028255
6 · The paper itself

Abstract

Acinar cells are the principal secretory units of multiple exocrine organs. A single-cell, layered, lumenized acinus forms from a large cohort of epithelial progenitors that must initiate and coordinate three cellular programs of acinar specification, namely, lineage progression, secretion, and polarization. Despite this well-known outcome, the mechanism(s) that regulate these complex programs are unknown. Here, we demonstrate that neuronal-epithelial cross-talk drives acinar specification through neuregulin (NRG1)-ERBB3-mTORC2 signaling. Using single-cell and global RNA sequencing of developing murine salivary glands, we identified NRG1-ERBB3 to precisely overlap with acinar specification during gland development. Genetic deletion of Erbb3 prevented cell lineage progression and the establishment of lumenized, secretory acini. Conversely, NRG1 treatment of isolated epithelia was sufficient to recapitulate the development of secretory acini. Mechanistically, we found that NRG1-ERBB3 regulates each developmental program through an mTORC2 signaling pathway. Thus, we reveal that a neuronal-epithelial (NRG1/ERBB3/mTORC2) mechanism orchestrates the creation of functional acini.

Indexed as

NeuregulinsSignal TransductionAcinar CellsAnimalsBiological TransportHumansMechanistic Target of Rapamycin Complex 2MiceNeuregulin-1Receptor, ErbB-3ERBB3 protein, humanMechanistic Target of Rapamycin Complex 2Neuregulin-1NeuregulinsNRG1 protein, humanNrg1 protein, mouseReceptor, ErbB-3acinusERBB3mTORneuregulinneuronal-epithelial communicationorganogenesissecretoryspecification

Identifiers

PMID36413949
PMCPMC9727910
OpenAlexW4309770471

What OpenQuestion holds

Textmetadata
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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.