Evidence map›Paper›PMID 34932949›Full record

ArticleDevelopmental cell2021

Endoderm development requires centrioles to restrain p53-mediated apoptosis in the absence of ERK activity.

Chang Xie, Shaun R Abrams, Vicente Herranz-Pérez, Jose Manuel García-Verdugo, Jeremy F Reiter

Open access · bronzeAbstract read
In one paragraph

Article in Developmental cell, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing 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

16 citing papers in PubMed, 22 citations in OpenAlex.

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  15. SOX2 and SOX21 in Lung Epithelial Differentiation and Repair.International journal of molecular sciences · 2022
    Review
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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

5 authors at 2 institutions in 2 countries.

Chang XieDepartment of Biochemistry and Biophysics, Cardiovascular Research Institute, University of California, San Francisco, San Francisco, CA, USA.
Shaun R AbramsDepartment of Biochemistry and Biophysics, Cardiovascular Research Institute, University of California, San Francisco, San Francisco, CA, USA.
Vicente Herranz-PérezCavanilles Institute of Biodiversity and Evolutionary Biology, University of Valencia, Valencia, Spain; Predepartamental Unit of Medicine, Jaume I University, Castelló de la Plana, Spain.
Jose Manuel García-VerdugoCavanilles Institute of Biodiversity and Evolutionary Biology, University of Valencia, Valencia, Spain.
Jeremy F ReiterDepartment of Biochemistry and Biophysics, Cardiovascular Research Institute, University of California, San Francisco, San Francisco, CA, USA; Chan Zuckerberg Biohub, San Francisco, CA 94158, USA. Electronic address: jeremy.reiter@ucsf.edu.
University of California, San Francisco · USUniversitat de València · ES

Funding

Hedgehog signaling at the cell's antenna: Smoothened and the primary ciliumR01AR054396 · NIAMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI Jeremy F Reiter · 2007 to 2026
$9.0M
Transition zone control of ciliary signalingR01GM095941 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI REITER, JEREMY F · 2011 to 2018
$3.4M
Understanding Ciliary Functions in Mammalian DevelopmentR01HD089918 · NICHD · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI REITER, JEREMY F, YODER, BRADLEY K. · 2017 to 2021
$3.0M
Transition zone control of ciliary signalingR01DE029454 · NIDCR · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI REITER, JEREMY F · 2019 to 2022
$2.3M
NIAMS NIH HHS R01 AR054396NICHD NIH HHS R01 HD089918NIDCR NIH HHS R01 DE029454NIGMS NIH HHS R01 GM095941
6 · The paper itself

Abstract

Centrioles comprise the heart of centrosomes, microtubule-organizing centers. To study the function of centrioles in lung and gut development, we genetically disrupted centrioles throughout the mouse endoderm. Surprisingly, removing centrioles from the endoderm did not disrupt intestinal growth or development but blocked lung branching. In the lung, acentriolar SOX2-expressing airway epithelial cells apoptosed. Loss of centrioles activated p53, and removing p53 restored survival of SOX2-expressing cells, lung branching, and mouse viability. To investigate how endodermal p53 activation specifically killed acentriolar SOX2-expressing cells, we assessed ERK, a prosurvival cue. ERK was active throughout the intestine and in the distal lung buds, correlating with tolerance to centriole loss. Pharmacologically inhibiting ERK activated apoptosis in acentriolar cells, revealing that ERK activity protects acentriolar cells from apoptosis. Therefore, centrioles are largely dispensable for endodermal growth and the spatial distribution of ERK activity in the endoderm shapes the developmental consequences of centriolar defects and p53 activation.

Indexed as

ApoptosisAnimalsCell SurvivalCentriolesEndodermEpithelial CellsExtracellular Signal-Regulated MAP KinasesIntestinesLungMiceMice, Inbred C57BLMicrotubule-Associated ProteinsMorphogenesisSOXB1 Transcription FactorsStem CellsTumor Suppressor Protein p53Cenpj protein, mouseExtracellular Signal-Regulated MAP KinasesMicrotubule-Associated ProteinsSOXB1 Transcription FactorsTumor Suppressor Protein p53apoptosiscentrioleendodermERKintestine developmentlung branchingp53

Identifiers

PMID34932949
PMCPMC8797031
OpenAlexW4200542570

What OpenQuestion holds

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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.