The Myb gene family was discovered due to the presence of the v-Myb oncogene in avian myeloblastosis virus. This retrovirus causes a rapidly fatal myeloid leukemia in the chicken.
The v-Myb oncogene is a transduced (stolen) partial copy of a highly conserved normal cellular gene called c-Myb.
Our laboratory spent many years developing biological assays for molecular clones of v-Myb and c-Myb.
We also developed biochemical assays for the v-Myb and c-Myb proteins encoded by these genes. The v-Myb and c-Myb proteins localize within the nucleus of the cell, bind directly to DNA, and can regulate gene expression. We used a variety of experimental approaches to explore the mechanism by which v-Myb and altered forms of c-Myb can transform normal blood cells into leukemic cancer cells. Mutated (genetically altered) forms of the human c-Myb gene cause human leukemia, brain cancer, breast cancer, and salivary gland cancer. Alterations of two closely related human genes, A-Myb and B-Myb, also cause various types of human cancer.
In recent years we have focused on Drosophila melanogaster (the fruit fly) as a model system because of the powerful genetic, genomic, and cell biological tools available in this organism. In addition, there is much less genetic redundancy in Drosophila than in mammals. In particular, Drosophila have one Myb gene, two E2F genes, and two Rb genes, whereas humans and other vertebrate animals have three Myb genes, eight E2F genes, and three Rb genes. Drosophila Myb is required for normal progression of the cell division cycle. In the absence of Myb, there are defects in chromosome condensation, assembly of the mitotic spindle, attachment of chromosomes to the spindle, and cytokinesis. Defective cytokinesis results in cells that contain more than one nucleus.
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