Role of the Pbrm1 subunit and the PBAF complex in Schwann cell development.
Animals
Cell Differentiation
/ genetics
Cell Lineage
/ genetics
Cell Proliferation
/ genetics
Cell Survival
/ genetics
Chromosomal Proteins, Non-Histone
/ physiology
DNA Helicases
/ genetics
DNA-Binding Proteins
/ physiology
Gene Deletion
Mice
Myelin Sheath
/ physiology
Nuclear Proteins
/ genetics
Peripheral Nerves
/ physiology
Schwann Cells
/ physiology
Transcription Factors
/ genetics
Journal
Scientific reports
ISSN: 2045-2322
Titre abrégé: Sci Rep
Pays: England
ID NLM: 101563288
Informations de publication
Date de publication:
16 02 2022
16 02 2022
Historique:
received:
15
11
2021
accepted:
01
02
2022
entrez:
17
2
2022
pubmed:
18
2
2022
medline:
15
3
2022
Statut:
epublish
Résumé
Myelin sheath formation in the peripheral nervous system and the ensuing saltatory conduction rely on differentiated Schwann cells. We have previously shown that transition of Schwann cells from an immature into a differentiated state requires Brg1 that serves as the central energy generating subunit in two related SWI/SNF-type chromatin remodelers, the BAF and the PBAF complex. Here we used conditional deletion of Pbrm1 to selectively interfere with the PBAF complex in Schwann cells. Despite efficient loss of Pbrm1 early during lineage progression, we failed to detect any substantial alterations in the number, proliferation or survival of immature Schwann cells as well as in their rate and timing of terminal differentiation. As a consequence, postnatal myelin formation in peripheral nerves appeared normal. There were no inflammatory alterations in the nerve or other signs of a peripheral neuropathy. We conclude from our study that Pbrm1 and very likely the PBAF complex are dispensable for proper Schwann cell development and that Schwann cell defects previously observed upon Brg1 deletion are mostly attributable to altered or absent function of the BAF complex.
Identifiants
pubmed: 35173232
doi: 10.1038/s41598-022-06588-8
pii: 10.1038/s41598-022-06588-8
pmc: PMC8850583
doi:
Substances chimiques
Chromosomal Proteins, Non-Histone
0
DNA-Binding Proteins
0
Nuclear Proteins
0
Pbrm1 protein, mouse
0
SWI-SNF-B chromatin-remodeling complex
0
Transcription Factors
0
Smarca4 protein, mouse
EC 3.6.1.-
DNA Helicases
EC 3.6.4.-
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
2651Informations de copyright
© 2022. The Author(s).
Références
Elife. 2021 Apr 23;10:
pubmed: 33890853
Brain Res. 2016 Jun 15;1641(Pt A):101-110
pubmed: 26423937
Elife. 2017 Dec 14;6:
pubmed: 29239726
J Cell Biol. 2010 May 17;189(4):701-12
pubmed: 20457761
Biochimie. 2009 Mar;91(3):309-19
pubmed: 19084573
J Neurosci. 2015 Jan 7;35(1):21-35
pubmed: 25568100
Nucleic Acids Res. 2020 Sep 18;48(16):8959-8976
pubmed: 32672815
PLoS One. 2013 Jul 16;8(7):e69037
pubmed: 23874858
J Biol Chem. 1996 Jul 19;271(29):17512-8
pubmed: 8663425
Genes Dev. 2004 Dec 15;18(24):3106-16
pubmed: 15601824
Nature. 2001 Dec 20-27;414(6866):924-8
pubmed: 11780067
Nat Commun. 2019 May 29;10(1):2361
pubmed: 31142747
Glia. 2008 Nov 1;56(14):1541-51
pubmed: 18803322
Genes Dev. 2003 Jun 1;17(11):1380-91
pubmed: 12782656
Cell. 2013 Jan 17;152(1-2):248-61
pubmed: 23332759
Nat Methods. 2012 Jun 28;9(7):676-82
pubmed: 22743772
Sci Adv. 2015 Jun 12;1(5):e1500447
pubmed: 26601204
Neuroscientist. 2018 Dec;24(6):627-638
pubmed: 29307265
Dev Cell. 2012 Jul 17;23(1):193-201
pubmed: 22814607
ACS Chem Biol. 2017 Oct 20;12(10):2482-2490
pubmed: 28921948
J Neurosci. 2012 Feb 1;32(5):1517-27
pubmed: 22302795
BMC Immunol. 2012 Feb 15;13:9
pubmed: 22336179
Dev Biol. 2005 Jan 1;277(1):155-69
pubmed: 15572147
Glia. 2020 Aug;68(8):1596-1603
pubmed: 31837180