Evidence map›Paper›PMID 36693323›Full record

ArticleDevelopmental cell2023

A cellular hierarchy of Notch and Kras signaling controls cell fate specification in the developing mouse salivary gland.

Lemonia Chatzeli, Ignacio Bordeu, Seungmin Han, Sara Bisetto, Zahra Waheed, Bon-Kyoung Koo, Maria P Alcolea, Benjamin D Simons

Open access · hybridAbstract read
In one paragraph

Article in Developmental cell, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing 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

14 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

8 authors at 3 institutions in 3 countries.

Lemonia ChatzeliWellcome Trust, Cancer Research UK Gurdon Institute, University of Cambridge, Cambridge CB2 1QN, UK; Wellcome Trust-Medical Research Council Cambridge Stem Cell Institute, Jeffrey Cheah Biomedical Centre, University of Cambridge, Cambridge CB2 0AW, UK. Electronic address: lc717@cam.ac.uk.
Ignacio BordeuWellcome Trust, Cancer Research UK Gurdon Institute, University of Cambridge, Cambridge CB2 1QN, UK; Department of Applied Mathematics and Theoretical Physics, Centre for Mathematical Sciences, University of Cambridge, Cambridge CB3 0WA, UK; Departamento de Física, Facultad de Ciencias Físicas y Matemáticas, Universidad de Chile, 837.0415 Santiago, Chile.
Seungmin HanWellcome Trust, Cancer Research UK Gurdon Institute, University of Cambridge, Cambridge CB2 1QN, UK; Wellcome Trust-Medical Research Council Cambridge Stem Cell Institute, Jeffrey Cheah Biomedical Centre, University of Cambridge, Cambridge CB2 0AW, UK.
Sara BisettoWellcome Trust-Medical Research Council Cambridge Stem Cell Institute, Jeffrey Cheah Biomedical Centre, University of Cambridge, Cambridge CB2 0AW, UK.
Zahra WaheedWellcome Trust-Medical Research Council Cambridge Stem Cell Institute, Jeffrey Cheah Biomedical Centre, University of Cambridge, Cambridge CB2 0AW, UK.
Bon-Kyoung KooCenter for Genome Engineering, Institute for Basic Science, Expo-ro 55, Yuseong-gu, Daejeon 34126, Republic of Korea.
Maria P AlcoleaWellcome Trust-Medical Research Council Cambridge Stem Cell Institute, Jeffrey Cheah Biomedical Centre, University of Cambridge, Cambridge CB2 0AW, UK; Department of Oncology, The Hutchison Building, Box 197 Cambridge Biomedical Campus, University of Cambridge, Cambridge, CB2 0XZ, UK.
Benjamin D SimonsWellcome Trust, Cancer Research UK Gurdon Institute, University of Cambridge, Cambridge CB2 1QN, UK; Wellcome Trust-Medical Research Council Cambridge Stem Cell Institute, Jeffrey Cheah Biomedical Centre, University of Cambridge, Cambridge CB2 0AW, UK; Department of Applied Mathematics and Theoretical Physics, Centre for Mathematical Sciences, University of Cambridge, Cambridge CB3 0WA, UK. Electronic address: bds10@cam.ac.uk.
Wellcome/MRC Cambridge Stem Cell Institute · GBInstitute for Basic Science · KRUniversity of Cambridge · GB

Funding

Cancer Research UK 23363Medical Research Council MC_PC_17230Medical Research Council MR/P019013/1Wellcome Trust 098357Wellcome Trust 098357/Z/12/ZWellcome Trust 219478Wellcome Trust 219478/Z/19/Z
6 · The paper itself

Abstract

The development of the mouse salivary gland involves a tip-driven process of branching morphogenesis that takes place in concert with differentiation into acinar, myoepithelial, and ductal (basal and luminal) sub-lineages. By combining clonal lineage tracing with a three-dimensional (3D) reconstruction of the branched epithelial network and single-cell RNA-seq analysis, we show that in tips, a heterogeneous population of renewing progenitors transition from a Krt14+ multipotent state to unipotent states via two transcriptionally distinct bipotent states, one restricted to the Krt14+ basal and myoepithelial lineage and the other to the Krt8+ acinar and luminal lineage. Using genetic perturbations, we show how the differential expression of Notch signaling correlates with spatial segregation, exits from multipotency, and promotes the Krt8+ lineage, whereas Kras activation promotes proacinar fate. These findings provide a mechanistic basis for how positional cues within growing tips regulate the process of lineage segregation and ductal patterning.

Indexed as

Signal TransductionStem CellsAnimalsCell DifferentiationCell LineageEpithelial CellsMiceSalivary GlandsacinibranchingdevelopmentdifferentiationductKrasKrt14Notchpotencysalivary gland

Identifiers

PMID36693323
PMCPMC7614884
OpenAlexW4318026450

What OpenQuestion holds

Textmetadata
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.