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. 2014 Dec 18;10(12):e1004768. doi: 10.1371/journal.pgen.1004768

Figure 7. Model of the collaboration between the SCL, LMO1 and Notch1 oncogenes.

Figure 7

(A) SCL and LMO1 interact to upregulate Lyl1 gene expression and create a feed forward loop that activates self-renewal in DN3 thymocytes. DN3 cells are prone to SCL-LMO1 self-renewal activity due to higher physiological NOTCH levels. (B) The Notch1 oncogene drastically enhances SCL-LMO1-induced self-renewal activity to expand the pool of target cells to DN1-4 and ISP8 in a parallel pathway via Hes1 and c-Myc. SCL-LMO1 initiated cells (A) subsequently acquire gain of function Notch1 mutations (B), causing target cell expansion and escape from thymic environmental control.