摘要
N6-adenosine methylation (m^(6)A) is the most abundant modification observed in mRNA transcripts. It is a dynamic modification that is performed by members of the so-called writer complex (including Wtap, Virma and Mettl3) and that can be removed by so-called eraser proteins [1]. In addition, m^(6)A is recognized by reader proteins (including Ythdf2) that can exert a response. Readers and m^(6)A can modify virtually all mRNA processes, including RNA splicing, secondary structures, nuclear export and transcript stability [1]. The functional relevance of m^(6)A-mediated regulation in specific cell types and treatment conditions remains only partly understood. In T cells, earlier studies have demonstrated a relevant role for m^(6)A in T effector (Teff), T follicular helper (TFH) and T regulatory (Treg) cells through manipulation of m^(6)A pathway genes in mice [2,3,4,5,6]. In these studies, disruption of m^(6)A resulted in dysregulation of gene expression patterns and caused colitis and systemic autoinflammatory disease. In a recent study by Ito-Kureha et al., the authors set out to further understand how m^(6)A signaling affects T-cell functions by manipulating Wtap in select T cells with a murine knockout model [7]. They found that m^(6)A signaling controls many aspects of T-cell immunobiology: activation, proliferation, life, and death.
