Protein truncation is not required for c-myb proto-oncogene activity in neuroretina cells.

AUTOR(ES)

Garrido, C

RESUMO

The v-myb oncogene of avian myeloblastosis virus (AMV) differs from its normal cellular counterpart by a truncation at both its amino and carboxyl termini and by a substitution of 11 amino acid residues. We had previously shown that v-myb-containing AMV, in the presence of basic fibroblast growth factor, transformed chicken neuroretina (CNR) cells. To understand the mechanism of c-myb activation, we have tested whether avian retroviruses that express the full-length c-Myb are also active on CNR cells. We have found that c-Myb, like v-Myb, strongly increases the basic fibroblast growth factor response of CNR cells and that these c-myb-expressing cells are able to grow in soft agar in the presence of the growth factor. We have also found that, in contrast to normal or v-myb-expressing AMV-transformed CNR cells, c-Myb-transformed cells express mim-1, a granulocyte-specific gene. However, normal v-Myb- and c-Myb-expressing CNR cells all express the pax-QNR gene, a newly described paired and homeobox-containing gene specifically expressed in the neuroretina. We conclude that, in contrast to what has been described for hematopoietic cells, overexpression of c-Myb is sufficient to activate gene expression and to induce an abnormal behavior of CNR cells.

Documentos Relacionados

• Protein truncation is required for the activation of the c-myb proto-oncogene.
• Transcriptional trans-repression by the c-myb proto-oncogene product.
• Trans-activation by the c-myb proto-oncogene.
• Structure of the protein encoded by the chicken proto-oncogene c-myb.
• Retroviral insertional activation of the c-myb proto-oncogene in a Marek's disease T-lymphoma cell line.