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Inhibition of cellular differentiation by the SCL/tal oncoprotein:
transcriptional repression by an Id-like mechanism
AN Goldfarb and K Lewandowska
Institute of Pathology, Case Western Reserve University, Cleveland, OH
44106-4943.
In cases of T-cell acute lymphoblastic leukemia (T-ALL), the basic
helix-loop-helix (bHLH) oncogene SCL/tal undergoes frequent rearrangements
activating ectopic expression. Despite the compelling epidemiological
association of SCL/tal expression with T-ALL, no specific transforming
function has been attributable to the protein product. However,
investigators have recently demonstrated that forced overexpression of
SCL/tal can block monocytic differentiation of M1 murine myeloid leukemia
cells. Thus, inappropriate expression of wild- type SCL/tal protein may in
part account for the maturation arrest phenotype observed in T-ALL cells.
In this study, ectopic expression of the SCL/tal gene blocked the
differentiation of C2C12 muscle precursor cells. Characterization of the
mechanism of differentiation blockade showed that the SCL/tal protein
repressed transcriptional activation by the myogenic bHLH factor MyoD.
Protein interaction analysis showed that SCL/tal and MyoD compete for
common partners (E bHLH proteins) but do not directly bind one other. A
model is thus proposed in which ectopic SCL/tal protein, by its ability to
titrate out E proteins, prevents the formation of bHLH complexes that drive
cellular differentiation: the "Id-like" mechanism.
Volume 85,
Issue 2,
pp. 465-471,
01/15/1995
Copyright © 1995 by The American Society of Hematology
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