Abstract:
The TAL1 gene has been localized to chromosome 1 and codes for a 47 kDa protein that acts as a transcription factor. Mutations involving TAL1 have been implicated in T-cell acute lymphoblastic leukemia (T-ALL). At the same time, another gene, called LMO1 is also active in this disease and also codes for a transcription factor. To further characterize how these genes influence the progression of T-ALL, NIH 3T3 cells, which do not normally express TAL1 or LMO1, were transfected with these transgenes to establish four different populations: a control, a LMO1-expressing cell population, a TAL1-expressing cell population, and a cell population containing both TAL1 and LMO1. These four populations were subsequently examined for their influence on expression of the cell cycle regulatory proteins cyclin D-1, p53, and Bcl-2 under normal and apoptotic conditions. All three proteins were expressed fairly equally among all four normal populations, however upon serum withdrawal, a differential expression of p53 was observed, and a complete lack of cyclin D-1 and Bcl-2 was observed in the control and TAL1 only cell populations. These results suggest that LMO1 may stabilize or promote the expression of thee proteins and lend a protective advantage to cells undergoing apoptosis, which allows them to continue to survive under limiting conditions.
