Evidence map›Paper›PMID 34336815›Full record

ArticleFrontiers in cell and developmental biology2021

Conditional Loss of BAF (mSWI/SNF) Scaffolding Subunits Affects Specification and Proliferation of Oligodendrocyte Precursors in Developing Mouse Forebrain.

Eman Abbas, Mohamed A Hassan, Godwin Sokpor, Kamila Kiszka, Linh Pham, Cemil Kerimoglu, Andre Fischer, Huu Phuc Nguyen, Jochen F Staiger, Tran Tuoc

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cell and developmental biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

8 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
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  3. Chromatin remodeling in tissue stem cell fate determination.Cell regeneration (London, England) · 2024
    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

10 authors at 5 institutions in 2 countries.

Eman AbbasInstitute for Neuroanatomy, University Medical Center, Georg-August-University Göttingen, Göttingen, Germany.
Mohamed A HassanProtein Research Department, Genetic Engineering and Biotechnology Research Institute (GEBRI), City of Scientific Research and Technological Applications (SRTA-City), New Borg El-Arab City, Egypt.
Godwin SokporInstitute for Neuroanatomy, University Medical Center, Georg-August-University Göttingen, Göttingen, Germany.
Kamila KiszkaInstitute for Neuroanatomy, University Medical Center, Georg-August-University Göttingen, Göttingen, Germany.
Linh PhamInstitute for Neuroanatomy, University Medical Center, Georg-August-University Göttingen, Göttingen, Germany.
Cemil KerimogluGerman Center for Neurodegenerative Diseases, Göttingen, Germany.
Andre FischerGerman Center for Neurodegenerative Diseases, Göttingen, Germany.
Huu Phuc NguyenProtein Research Department, Genetic Engineering and Biotechnology Research Institute (GEBRI), City of Scientific Research and Technological Applications (SRTA-City), New Borg El-Arab City, Egypt.
Jochen F StaigerInstitute for Neuroanatomy, University Medical Center, Georg-August-University Göttingen, Göttingen, Germany.
Tran TuocInstitute for Neuroanatomy, University Medical Center, Georg-August-University Göttingen, Göttingen, Germany.
Ruhr University Bochum · DEUniversity of Göttingen · DECity of Scientific Research and Technological Applications · EGGerman Center for Neurodegenerative Diseases · DEUniversitätsmedizin Göttingen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oligodendrocytes are responsible for axon myelination in the brain and spinal cord. Generation of oligodendrocytes entails highly regulated multistage neurodevelopmental events, including proliferation, differentiation and maturation. The chromatin remodeling BAF (mSWI/SNF) complex is a notable regulator of neural development. In our previous studies, we determined the indispensability of the BAF complex scaffolding subunits BAF155 and BAF170 for neurogenesis, whereas their role in gliogenesis is unknown. Here, we show that the expression of BAF155 and BAF170 is essential for the genesis of oligodendrocytes during brain development. We report that the ablation of BAF155 and BAF170 in the dorsal telencephalic (dTel) neural progenitors or in oligodendrocyte-producing progenitors in the ventral telencephalon (vTel) in double-conditional knockout (dcKO) mouse mutants, perturbed the process of oligodendrogenesis. Molecular marker and cell cycle analyses revealed impairment of oligodendrocyte precursor specification and proliferation, as well as overt depletion of oligodendrocytes pool in dcKO mutants. Our findings unveil a central role of BAF155 and BAF170 in oligodendrogenesis, and thus substantiate the involvement of the BAF complex in the production of oligodendrocytes in the forebrain.

Indexed as

BAF155 and BAF170BAF complexoligodendrocyte developmentoligodendrogenesisOPC specification and proliferation

Identifiers

PMID34336815
PMCPMC8320002
OpenAlexW3185440378

What OpenQuestion holds

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LicenceCC BY
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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.