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Vol. 17, No. 8, pp. 959-964, April 15, 2003
1 Max-Delbrück-Center for Molecular Medicine, Berlin,
Germany; 2 Laboratory of Hemopoiesis and Leukemia, Clinical
Research Institute of Montreal, Montreal, Quebec H2W 1R7, Canada.
We investigated the translational regulation of SCL protein
expression and its role in hematopoietic lineage choice. We show that
the expression of different SCL protein isoforms is regulated by signal
transduction pathways that modulate translation initiation factor (eIF)
function. A conserved small upstream open reading frame (uORF) in SCL
transcripts acts as a cis-regulatory element for isoform
expression. At the onset of erythroid differentiation, truncated SCL
protein isoforms arise by alternative translation initiation and favor
the erythroid lineage. In comparison, full-length SCL proteins are more
efficient at enhancing the megakaryocyte lineage. Together, our studies
unravel translational control as a novel mechanism regulating
hematopoietic outcome.
[Keywords:
Hematopoiesis; lineage commitment; translation initiation; uORF; eIF4E; eIF2
]
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