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. Author manuscript; available in PMC: 2015 Mar 1.
Published in final edited form as: Semin Cell Dev Biol. 2014 Jan 24;0:86–95. doi: 10.1016/j.semcdb.2014.01.006

Figure 1. Mutagenic transposon vector for gain- and loss- of-function screen.

Figure 1

(A) The mutagenic T2/Onc transposon contains splice acceptors (SAs) followed by polyadenylation (pA) signals in both orientations, which are designed to elicit premature transcript truncation. The 5′-long terminal repeat (LTR) of the murine stem cell virus (MSCV) fused with a splice donor (SD) was placed in between the two SAs to drive misexpression of genes. This MSCV contains enhancer and strong cis-regulatory elements that have been shown to be active and methylation-resistant in pluripotent cells. IR/DR, inverted repeat/direct terminal repeat sequences. (B) Gain-of-function screen for proto-oncogenes. The mutagenic transposon vector can integrate upstream of a proto-oncogene and cause misexpression or create truncated versions by integrating within intronic sequences of the endogenous gene. (C) Loss-of-function screen for tumor suppressor genes. The mutagenic transposon vector can integrate within intronic sequences and disrupt expression of tumor suppressor genes.