The gene SCL is expressed during early hematopoiesis and encodes a differentiation-related DNA-binding motif.

Abstract

We have identified the human gene, SCL. We discovered this gene because of its involvement in a chromosomal translocation associated with the occurrence of a stem cell leukemia manifesting myeloid and lymphoid differentiation capabilities. Here we report the sequence of a cDNA for the normal SCL transcript, as well as for an aberrant fusion transcript produced in the leukemic cells. Although different at their 3' untranslated regions, both cDNAs predict a protein with primary amino acid sequence homology to the previously described amphipathic helix-loop-helix DNA binding and dimerization motif of the Lyl-1, myc, MyoD, immunoglobulin enhancer binding, daughterless, and achaete-scute families of genes. For these cDNAs, at least two different 5' ends are predicted, both of which retain this putative DNA binding domain and predict proteins in the range of 20-30 kDa. SCL mRNA is observed in "early" hematopoietic tissues. Taken together, these studies lead to the speculation that SCL plays a role in differentiation and/or commitment events during hematopoiesis.

The CD2-scl transgene alters the phenotype and frequency of T-lymphomas in N-ras transgenic or p53 deficient mice

“…Three cases displayed a normal CD4+ phenotype (Figure 5b) while one lymphoma arising from a cervical lymph node expressed an unusual combination of both CD4 and the B-cell marker, B220 (Figure 5c). Co-expression of B and T-cell surface markers is consistent with the phenotype of the ®rst leukemia in which SCL was de®ned (Begley et al, 1989). However, dual staining for CD4 and B220 was not performed and thus a mixture of mature T-cells and pre-B cells could not be excluded.…”

“…The SCL (TAL-1/TCL5) gene was ®rst identi®ed by its involvement in a t(1;14)(p32;q11) chromosomal translocation seen in 3% of childhood T-cell acute lymphoblastic leukemia (T-ALL) (Begley et al, 1989;Finger et al, 1989;Chen et al, 1990). Scl is a member of the basic helix ± loop ± helix (bHLH) family of transcription factors.…”

p300 functions as a transcriptional coactivator for the TAL1/SCL oncoprotein

“…TAL1 transcripts and protein have been detected in a number of hematopoietic, as well as certain nonhematopoietic, cell types (Begley et al, 1989b;Green et al, 1991Green et al, , 1992Hwang et al, 1993;Kallianpur et al, 1994;Mouthon et al, 1993;Pulford et al, 1995;Visvader et al, 1991), and its expression in embryonic development pre®gures and parallels sites of blood formation (Kallianpur et al, 1994). Further, mouse embryos homozygous for a targeted mutation in Tal1 died in midgestation with the complete absence of yolk sac blood cells (Robb et al, 1995;Shivdasani et al, 1995).…”

GOOSECOID inhibits erythrocyte differentiation by competing with Rb for PU.1 binding in murine cells

“…Many transcription factors are thought to play a role in erythropoiesis, such as GATA-1 (Kulessa et al, 1995;Tsai et al, 1991), GATA-2 (Tsai et al, 1994), PU.1 (Hromas et al, 1993;Schuetze et al, 1992Schuetze et al, , 1993 and SCL (Aplan et al, 1992;Begley et al, 1989;Shivdasani and Orkin, 1996). Among these, the role of PU.1 in erythropoiesis is still controversial.…”