Tet2 is required for Socs activation in immune response cells [ChIP-seq]

Purpose: We have previously established an in vitro murine model that recapitulates the transformed phenotype of primary Tet2-/- mast cells expressing the Kit kinase domain mutant allele, D816V, that is both an oncogene and characterises patients with mastocytosis. To better understand the molecular basis of this cooperation and to further our understanding of role of Tet2 during inflammation and in other immune system disorders, we used this same in vitro primary cell system for genome wide studies to identify genes and genomic loci that are deregulated when these two mutations cooperate in mast cells. ChIP-seq was performed on biological replicates with each ChIp antibody on 4 paired samples: 1) GFP-negative/control and 2) GFP-positive/KitD816V infected Tet2+/+ mast cells, and 3) GFP-negative/control and 4) GFP-positive/KitD816V infected Tet2-/- mast cells. Biological replicates constitute primary mast cell cultures derived from two individual mice of each genotype, cultured in parallel.