m6A mRNA methylation sustains Treg suppressive functions

TONG, JIYU; CAO, GUANGCHAO; ZHANG, TING; SEFIK, ESEN; AMEZCUA VESELY, MARIA CAROLINA; BROUGHTON, JAMES P; ZHU, SHU; LI, HUABIN; LI, BIN; CHEN, LEI; CHANG, HOWARD Y; SU, BING; FLAVELL, RICHARD A; LI, HUA-BING

CELL RESEARCH

NATURE PUBLISHING GROUP

Año: 2018 vol. 28 p. 253 - 253

1001-0602

6-methyladenosine (m6A) is the most abundant mRNA chemical modification, and is modulated by m6A ?writers?, ?erasers? and ?readers? proteins [1-3]. In vitro experiments suggest that m6A regulates several aspects of RNA metabolism, including RNA decay, splicing and translation [1]. Recent genetic analyses in vivo showed that m6A functions in sex determination in Drosophila [4, 5], in maternal-to-zygotic transition and haematopoietic stem cell specification during zebrafish embryogenesis [6, 7], in mouse spermatogenesis [8-10], and in mouse brain development [11]. We recently discovered that lin- eage-specific deletion of the m6A ?writer? enzyme MET- TL3 in CD4+ T cells (Mettl3f/f; CD4-Cre) led to disrup- tion of naïve T cell homeostasis [12]. CD4+ regulatory T cells (Tregs) comprise a critical subset of effector T cells, which are involved in resolution of inflammation and immunosuppression in tumor microenvironments [13]. However, the potential roles of m6A mRNA modification in Treg f