Ezh2 programs TFH differentiation by integrating phosphorylation-dependent activation of Bcl6 and polycomb-dependent repression of p19Arf

Fengyin Li; Zhouhao Zeng; Shaojun Xing; Jodi A. Gullicksrud; Qiang Shan; Jinyong Choi; Vladimir P. Badovinac; Shane Crotty; Weiqun Peng; Hai-Hui Xue

doi:10.1038/s41467-018-07853-z

Nature Communications (Dec 2018)

Ezh2 programs TFH differentiation by integrating phosphorylation-dependent activation of Bcl6 and polycomb-dependent repression of p19Arf

Fengyin Li,
Zhouhao Zeng,
Shaojun Xing,
Jodi A. Gullicksrud,
Qiang Shan,
Jinyong Choi,
Vladimir P. Badovinac,
Shane Crotty,
Weiqun Peng,
Hai-Hui Xue

Affiliations

Fengyin Li: Institutes for Translational Medicine, Soochow University
Zhouhao Zeng: Department of Physics, The George Washington University
Shaojun Xing: Department of Microbiology and Immunology, Carver College of Medicine, University of Iowa
Jodi A. Gullicksrud: Department of Microbiology and Immunology, Carver College of Medicine, University of Iowa
Qiang Shan: Department of Microbiology and Immunology, Carver College of Medicine, University of Iowa
Jinyong Choi: La Jolla Institute
Vladimir P. Badovinac: Department of Microbiology and Immunology, Carver College of Medicine, University of Iowa
Shane Crotty: La Jolla Institute
Weiqun Peng: Department of Physics, The George Washington University
Hai-Hui Xue: Department of Microbiology and Immunology, Carver College of Medicine, University of Iowa

DOI: https://doi.org/10.1038/s41467-018-07853-z
Journal volume & issue: Vol. 9, no. 1
pp. 1 – 18

Abstract

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Ezh2 is an histone methyltransferase that catalyzes H3K27me3. Here the authors show that Ezh2 promotes T follicular helper (TFH) differentiation and helper activity, by cooperating with Tcf1 to activate Bcl6 transcription and epigenetically repressing p19Arf, an antagonist of Bcl6 function and TFH cell survival.

Published in Nature Communications

ISSN: 2041-1723 (Online)
Publisher: Nature Portfolio
Country of publisher: United Kingdom
LCC subjects: Science
Website: https://www.nature.com/ncomms/

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