γδ T cell is abundant T cell population and is critical in mucosal tissue homeostasis as well as immunoregulation, while its detailed developmental mechanisms remain poorly understood. Our previous studies have demonstrated N6-methyladenosine (m6A) plays important roles in controlling the homeostasis, differentiation and function of CD4+ αβ T cells, but whether it plays a role in γδ T cell biology is still unclear. Here we show that depletion of m6A demethylase ALKBH5 in lymphocytes specifically induces an expansion of γδ T cells, which confers enhanced protection against gastrointestinal S. typhimurium infection. Mechanistically, loss of ALKBH5 favors the development of γδ T cell precursors by increasing the abundance of m6A RNA modification in thymocytes, which further reduces the expression of several target genes including Notch signaling components Jagged1 and Notch2. As a result, impairment of Jagged1/Notch2 signaling contributes to enhanced proliferation and differentiation of γδ T cell precursors, leading to an expanded mature γδ T cell repertoire. Taken together, our results indicate a checkpoint role of ALKBH5 and m6A modification in the regulation of γδ T cell early development.