Transcriptome data of wt, Rbx1- or Ube2m- deficient Treg cells from mice

Cullin-RING Ligases (CRLs), upon activation by neddylation, play the key roles in regulating many biological processes. However, how CRL-neddylation regulates the function of Treg cells remains elusive. Here we show that mice with Treg-specific deletion of Rbx1, a RING component of CRLs required for its activity, developed an early-onset fetal inflammatory disorders and death at day ~25 after birth with disrupted homeostasis and impaired suppressive functions of Treg cells. Specifically, Rbx1 is essential for maintenance of the effector subpopulations in Treg cells, and regulates several inflammatory pathways. Similar phenotypes were seen in mice with deletion of Ube2m, a neddylation E2, in Treg cells, but with much lesser severity. Interestingly, Treg-specific deletion of Rbx2/Sag or Ube2f, the family member of Rbx1 or Ube2m, respectively, had no obvious phenotype. Thus, the Ube2m-Rbx1 axis is required for the maintenance of homeostasis and functions of Treg cells; and Rbx1 has Ube2m-independent roles in the fitness of Treg cells, suggesting a layer of complexity in neddylation activation of CRLs. We use the tranpritome dara to show the mechanism of the function of Rbx1 and Ube2m in Treg cells, also research the relationship of Rbx1 and Ube2m in Treg cells. CD4+YFP+ Treg cells were isolated from the peripheral lymph nodes and spleens of mice (8-12 weeks old) with indicated genotypes. To generate enough materials, the pooled tissues from 2-3 mice (Foxp3cre/wt), 8-11 (Foxp3cre/wt;Rbx1fl/fl) or 3-4 (Foxp3cre/wt;Ube2mfl/fl) were used. Each type of contains three biological replications.