The avian fli gene is specifically expressed during embryogenesis in a subset of neural crest cells giving rise to mesenchyme.

The ets-family of transcription factors is involved in the development of endothelial and hematopoietic cells. Among these genes, fliwas shown to be responsible for erythroblastomas and Ewing's sarcomas. Its involvement in Ewing's sarcoma, a putative neurectodermal tumor, as well as the in situ hybridization studies performed in mice and Xenopus suggested a role in neural crest development. We cloned quail fli cDNA in order to analyze in more detail its expression in neural crest cells, which have been extensively studied in avian species. Fli gene maps on chicken chromosome 1 to band q31->q33. Two RNAs are transcribed, most likely arising from two different promoters. The analysis of its expression in neural crest cells reveals that it is expressed rather late, when the neural crest cells reach their target. Among the various lineages derived from the crest, it is restricted to the mesenchymal one. It is maintained at later stages in the cartilage of neural crest but also of mesodermal origin. In addition, fli is expressed in several mesoderm-derived cells: endothelial cells as well as intermediate and splanchnopleural mesoderm.

Overexpression of the Xenopus Xl-fli gene during early embryogenesis leads to anomalies in head and heart development and erythroid differentiation.

The product of the Xl-fli gene, a Xenopus laevis transcription factor of the ets family, specifically expressed in several lineage of migratory cells during Xenopus development (Meyer et al., Int. J. Dev. Biol. 39: 909-919, 1995) was overproduced during Xenopus embryogenesis, upon microinjection of a synthetic transcript in the fertilized egg or in the early embryo. This results in anomalies of the antero-posterior and dorso-ventral polarities, and in tissue differentiation, particularly in the eye- and head cartilage development, as well as erythroid differentiation (absence of erythrocyte differentiation in the circulating blood, often accompanied by ectopic localization of mature erythrocytes, leading to important hemangiomas). Cytological examination reveals at gastrulation the existence of abnormal cells separating the different embryonic layers, suggesting modifications of the cellular adhesion properties. The possible involvement of the fli gene in controlling the dissemination of migratory cells is discussed.

Whole-mount in situ hybridization reveals the expression of the Xl-Fli gene in several lineages of migrating cells in Xenopus embryos.

The expression of the Xl-Fli gene, which belongs to the ets family of transcription factors, was studied by whole-mount in situ hybridization during Xenopus embryogenesis. Digoxigenin-labeled antisense RNA probes were synthesized by in vitro transcription and used in the hybridization reaction. In addition to expression in territories invaded by neural crest cells reported earlier (Meyer et al., 1993), we observed Xl-Fli gene expression in a number of regions affected by important cellular migrations and/or epithelium<==>mesenchyme transitions: in the endothelial cells of the heart, in blood vessels, along the pronephric duct migration pathway and at the level of hypophysis. The possibility that the FLI protein is involved in the expression of guidance cues and/or modification of the cellular adhesion properties is discussed. A screening of a promoter library with a consensus sequence, bound by the FLI protein with a high affinity, revealed the presence of putative FLI response elements in a number of genes encoding adhesion molecules or components of the extra-cellular matrix.