Evidence map›Paper›PMID 34994686›Full record

ArticleeLife2022

PRC1 sustains the integrity of neural fate in the absence of PRC2 function.

Ayana Sawai, Sarah Pfennig, Milica Bulajić, Alexander Miller, Alireza Khodadadi-Jamayran, Esteban O Mazzoni, Jeremy S Dasen

Open access · goldAbstract read
In one paragraph

Article in eLife, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing 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

15 citing papers in PubMed, 21 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

7 authors at 3 institutions in 2 countries.

Ayana SawaiNeuroscience Institute, Department of Neuroscience and Physiology, NYU School of Medicine, New York, United States.ORCID 0000-0002-5446-4930
Sarah PfennigNeuroscience Institute, Department of Neuroscience and Physiology, NYU School of Medicine, New York, United States.
Milica BulajićDepartment of Biology, New York University, New York, United States.
Alexander MillerNeuroscience Institute, Department of Neuroscience and Physiology, NYU School of Medicine, New York, United States.
Alireza Khodadadi-JamayranApplied Bioinformatics Laboratories, Office of Science and Research, NYU School of Medcine, New York, United States.
Esteban O MazzoniDepartment of Biology, New York University, New York, United States.ORCID 0000-0001-8994-681X
Jeremy S DasenNeuroscience Institute, Department of Neuroscience and Physiology, NYU School of Medicine, New York, United States.ORCID 0000-0002-9434-874X
Neuroscience Institute · ITNew York University · USOffice of Science · US

Funding

Genetic Control of Circuit Assembly in the Vertebrate Spinal Cord - Diversity SupplementR35NS116858 · NINDS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI JEREMY S DASEN · 2020 to 2026
$6.7M
Understanding CTCF Boundaries Controlling Hox Gene ExpressionR01NS100897 · NINDS · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI Esteban Orlando Mazzoni, DANNY REINBERG · 2018 to 2026
$4.1M
Transcriptional Control of Motor Neuron Identity and Connectivity. - Renewal - 1R01NS062822 · NINDS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI DASEN, JEREMY S · 2009 to 2019
$3.9M
TRAINING PROGRAM IN DEVELOPMENTAL GENETICS.T32HD007520 · NICHD · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI TREISMAN, JESSICA E · 1999 to 2023
$3.9M
GRADUATE PROGRAM IN CELLULAR &MOLECULAR BIOLOGYT32GM007238 · NIGMS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI RIFKIN, DANIEL B · 1985 to 2013
$2.7M
Genetic Control of Topographic Map Formation in the Development of Spinal CircuitsR01NS097550 · NINDS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI DASEN, JEREMY S · 2016 to 2019
$1.5M
Defining the mechanisms of Hox gene repression during motor neuron developmentF31NS087772 · NINDS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI SAWAI-FRANTZ, AYANA · 2014 to 2016
$116k
NICHD NIH HHS T32 HD007520NIGMS NIH HHS T32 GM007238NINDS NIH HHS F31 NS087772NINDS NIH HHS R01 NS062822NINDS NIH HHS R01 NS097550NINDS NIH HHS R01 NS100897NINDS NIH HHS R35 NS116858
6 · The paper itself

Abstract

Polycomb repressive complexes (PRCs) 1 and 2 maintain stable cellular memories of early fate decisions by establishing heritable patterns of gene repression. PRCs repress transcription through histone modifications and chromatin compaction, but their roles in neuronal subtype diversification are poorly defined. We found that PRC1 is essential for the specification of segmentally restricted spinal motor neuron (MN) subtypes, while PRC2 activity is dispensable to maintain MN positional identities during terminal differentiation. Mutation of the core PRC1 component

Indexed as

Gene Expression Regulation, DevelopmentalAnimalsAnimals, Genetically ModifiedChickensEmbryonic Stem CellsMiceMotor NeuronsPolycomb Repressive Complex 1Polycomb Repressive Complex 2Polycomb Repressive Complex 1Polycomb Repressive Complex 2chickendevelopmental biologyhox genemotor neuronmouseneural developmentneurosciencepolycomb protein

Identifiers

PMID34994686
PMCPMC8765755
OpenAlexW4205343992

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.