A Genome-wide CRISPR Screen Reveals a Role for the Non-canonical Nucleosome-Remodeling BAF Complex in Foxp3 Expression and Regulatory T Cell Function.


Journal

Immunity
ISSN: 1097-4180
Titre abrégé: Immunity
Pays: United States
ID NLM: 9432918

Informations de publication

Date de publication:
14 07 2020
Historique:
received: 20 02 2020
revised: 20 04 2020
accepted: 12 06 2020
pubmed: 9 7 2020
medline: 24 3 2021
entrez: 9 7 2020
Statut: ppublish

Résumé

Regulatory T (Treg) cells play a pivotal role in suppressing auto-reactive T cells and maintaining immune homeostasis. Treg cell development and function are dependent on the transcription factor Foxp3. Here, we performed a genome-wide CRISPR loss-of-function screen to identify Foxp3 regulators in mouse primary Treg cells. Foxp3 regulators were enriched in genes encoding subunits of the SWI/SNF nucleosome-remodeling and SAGA chromatin-modifying complexes. Among the three SWI/SNF-related complexes, the Brd9-containing non-canonical (nc) BAF complex promoted Foxp3 expression, whereas the PBAF complex was repressive. Chemical-induced degradation of Brd9 led to reduced Foxp3 expression and reduced Treg cell function in vitro. Brd9 ablation compromised Treg cell function in inflammatory disease and tumor immunity in vivo. Furthermore, Brd9 promoted Foxp3 binding and expression of a subset of Foxp3 target genes. Our findings provide an unbiased analysis of the genetic networks regulating Foxp3 and reveal ncBAF as a target for therapeutic manipulation of Treg cell function.

Identifiants

pubmed: 32640256
pii: S1074-7613(20)30266-1
doi: 10.1016/j.immuni.2020.06.011
pmc: PMC7341821
pii:
doi:

Substances chimiques

Brd9 protein, mouse 0
Forkhead Transcription Factors 0
Foxp3 protein, mouse 0
Nucleosomes 0
RNA, Guide 0
Transcription Factors 0

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

143-157.e8

Subventions

Organisme : NIH HHS
ID : S10 OD023689
Pays : United States
Organisme : NIAID NIH HHS
ID : R01 AI107027
Pays : United States
Organisme : NIGMS NIH HHS
ID : F32 GM128377
Pays : United States
Organisme : NCI NIH HHS
ID : P30 CA014195
Pays : United States
Organisme : NIAID NIH HHS
ID : R01 AI151123
Pays : United States
Organisme : NCI NIH HHS
ID : T32 CA009370
Pays : United States

Commentaires et corrections

Type : CommentIn

Informations de copyright

Copyright © 2020 Elsevier Inc. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of Interests A patent application has been filed based on the findings described in this study.

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Auteurs

Chin-San Loo (CS)

NOMIS Center for Immunobiology and Microbial Pathogenesis, Salk Institute for Biological Studies, La Jolla, CA, USA; Division of Biological Sciences, University of California, San Diego, La Jolla, CA, USA.

Jovylyn Gatchalian (J)

Molecular and Cellular Biology Laboratory, Salk Institute for Biological Studies, La Jolla, CA, USA.

Yuqiong Liang (Y)

NOMIS Center for Immunobiology and Microbial Pathogenesis, Salk Institute for Biological Studies, La Jolla, CA, USA.

Mathias Leblanc (M)

NOMIS Center for Immunobiology and Microbial Pathogenesis, Salk Institute for Biological Studies, La Jolla, CA, USA.

Mingjun Xie (M)

NOMIS Center for Immunobiology and Microbial Pathogenesis, Salk Institute for Biological Studies, La Jolla, CA, USA.

Josephine Ho (J)

Molecular and Cellular Biology Laboratory, Salk Institute for Biological Studies, La Jolla, CA, USA.

Bhargav Venkatraghavan (B)

NOMIS Center for Immunobiology and Microbial Pathogenesis, Salk Institute for Biological Studies, La Jolla, CA, USA.

Diana C Hargreaves (DC)

Molecular and Cellular Biology Laboratory, Salk Institute for Biological Studies, La Jolla, CA, USA. Electronic address: dhargreaves@salk.edu.

Ye Zheng (Y)

NOMIS Center for Immunobiology and Microbial Pathogenesis, Salk Institute for Biological Studies, La Jolla, CA, USA. Electronic address: yzheng@salk.edu.

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Classifications MeSH