Evidence map›Paper›PMID 31020615›Full record

ArticleMolecular neurobiology2019

RBM15 Modulates the Function of Chromatin Remodeling Factor BAF155 Through RNA Methylation in Developing Cortex.

Yuanbin Xie, Ricardo Castro-Hernández, Godwin Sokpor, Linh Pham, Ramanathan Narayanan, Joachim Rosenbusch, Jochen F Staiger, Tran Tuoc

Abstract read
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In one paragraph

Article in Molecular neurobiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
4.5field-weighted citation impact, top 4% 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

40 citing papers in PubMed, 78 citations in OpenAlex.

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  10. Exploring the role of mFrontiers in oncology · 2024
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  11. RNA binding proteins in cardiovascular development and disease.Current topics in developmental biology · 2024
    Article
  12. Review
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  15. Review
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  17. Article
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  19. Analysis and identification of mMolecular therapy. Nucleic acids · 2022
    Article
  20. RBM15 condensates modulate mComputational and structural biotechnology journal · 2022
    Article
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 2 countries.

Yuanbin XieInstitute for Neuroanatomy, University Medical Center, Georg-August-University Goettingen, 37075, Goettingen, Germany. yuanbin.xie@med.uni-goettingen.de.
Ricardo Castro-HernándezInstitute for Neuroanatomy, University Medical Center, Georg-August-University Goettingen, 37075, Goettingen, Germany.
Godwin SokporInstitute for Neuroanatomy, University Medical Center, Georg-August-University Goettingen, 37075, Goettingen, Germany.
Linh PhamInstitute for Neuroanatomy, University Medical Center, Georg-August-University Goettingen, 37075, Goettingen, Germany.
Ramanathan NarayananInstitute for Neuroanatomy, University Medical Center, Georg-August-University Goettingen, 37075, Goettingen, Germany.
Joachim RosenbuschInstitute for Neuroanatomy, University Medical Center, Georg-August-University Goettingen, 37075, Goettingen, Germany.
Jochen F StaigerInstitute for Neuroanatomy, University Medical Center, Georg-August-University Goettingen, 37075, Goettingen, Germany.
Tran TuocInstitute for Neuroanatomy, University Medical Center, Georg-August-University Goettingen, 37075, Goettingen, Germany. tran.tuoc@med.uni-goettingen.de.ORCID http://orcid.org/0000-0003-2079-7259
University of Göttingen · DENanoscale Microscopy and Molecular Physiology of the Brain Cluster of Excellence 171 — DFG Research Center 103 · DEETH Zurich · CH

Funding

DFG TU432/1-1, TU432/3-1DFG-CNMPB B1Schram-Stiftung 2017/273
6 · The paper itself

Abstract

Chromatin remodeling factor BAF155 is an important regulator of many biological processes. As a core and scaffold subunit of the BAF (SWI/SNF-like) complex, BAF155 is capable of regulating the stability and function of the BAF complex. The spatiotemporal expression of BAF155 during embryogenesis is essential for various aspects of organogenesis, particularly in the brain development. However, our understanding of the mechanisms that regulate the expression and function of BAF155 is limited. Here, we report that RBM15, a subunit of the m6A methyltransferase complex, interacts with BAF155 mRNA and mediates BAF155 mRNA degradation through the mRNA methylation machinery. Ablation of endogenous RBM15 expression in cultured neuronal cells and in the developing cortex augmented the expression of BAF155. Conversely, RBM15 overexpression decreased BAF155 mRNA and protein levels, and perturbed BAF155 functions in vivo, including repression of BAF155-dependent transcriptional activity and delamination of apical radial glial progenitors as a hallmark of basal radial glial progenitor genesis. Furthermore, we demonstrated that the regulation of BAF155 by RBM15 depends on the activity of the mRNA methylation complex core catalytic subunit METTL3. Altogether, our findings reveal a new regulatory avenue that elucidates how BAF complex subunit stoichiometry and functional modulation are achieved in mammalian cells.

Indexed as

Chromatin Assembly and DisassemblyAdenosineAdherens JunctionsAnimalsCell LineCerebral CortexHumansMethylationMethyltransferasesMiceModels, BiologicalNeurogliaRNARNA-Binding ProteinsRNA, MessengerTranscription FactorsAdenosineMethyltransferasesMettl3 protein, mouseN-methyladenosineRbm15 protein, mouseRNARNA-Binding ProteinsRNA, MessengerSmarcc1 protein, mouseTranscription FactorsBAF155BAF (mSWI/SNF) complexBasal progenitorCortical developmentMETTL3RBM15RNA decayRNA methylation

Identifiers

PMID31020615
OpenAlexW2941054016

What OpenQuestion holds

Textmetadata
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.