v-Myb can transform and regulate the differentiation of melanocyte precursors

Abstract

The activity of the c-Myb transcription factor is essential for the development of de®nitive multi-and uni-lineage progenitors of the haemopoietic system. Re¯ecting this requirement, c-Myb has been oncogenically activated by transduction in the E26 avian retrovirus which elicits an acute leukaemia by transforming haemopoietic progenitors. Here, we report the novel ®nding that Myb in cooperation with EGF receptor signalling can be used to generate clonally expanded populations of transformed cells which have the phenotype of melanocyte precursors. Through the use of a conditional temperature sensitive mutant of Myb, we show that in the transformed cells Myb regulates commitment to melanocyte di erentiation and possibly proliferation. These results add to our understanding of the roles of c-Myb beyond the haemopoietic system and to our knowledge and means of investigating the importance of transcription factors in the melanocyte linage.

The functional −443T/C osteopontin promoter polymorphism influences osteopontin gene expression in melanoma cells via binding of c‐Myb transcription factor

“…In line with this, a relation between FGF receptor signaling and v‐Myb‐dependent transcriptional regulation in melanocytic cells has been demonstrated earlier 48. It was shown that chicken chorioembryonic stem cells could be differentiated into melanoblasts by the simultaneous ectopic overexpression of both FGF receptor and v‐Myb.…”

Developmental gene expression profiling of mammalian, fetal orofacial tissue

“…The c ‐ myb protooncogene has been demonstrated to promote cell proliferation in cooperation with EGF receptor signaling (Bell and Frampton, 1999), in addition to its well known role in the hematopoietic system (Karafiat et al, 2001). In view of the observation that EGF is a potent mitogen for palate mesenchymal cells (Pisano and Greene, 1987; Potchinsky et al, 1998) and that a steady upregulation of c‐myb gene expression was seen from GD‐12 to GD‐14 in developing orofacial tissue, one might speculate that c‐myb acts in concert with EGF, promoting proliferation of various cell types, including palate mesenchymal cells, within the developing orofacial complex.…”

c-Myb a stem-progenitor cell regulator in multiple tissue compartments

“…However, c-myb expression appears to be required in a number of other tissue settings most notably in colonic crypts and neurogenic zones of the mouse. Compelling evidence that c-Myb is expressed and/or required in smooth muscle (Brown et al 1992, You et al 2003, melanocytes (Bell and Frampton 1999) and the epidermis (Ess et al 1999) has also been reported. Although recognized by Thompson et al (1986) nearly two decades ago, that c-myb expression is regulated in chick embryo fibroblasts (CEFs) and more recently, that when c-Myb function is inhibited mouse embryo fibroblasts (MEF) show retarded entry into the cell cycle (Bein et al 1997), the field in general has tended to partition these studies to one side.…”