Juan Santana will Present his Research on Wednesday, 4-8-15
DM-MYB REGULATION OF CELL CYCLE GENES IS INDEPENDENT OF NURF
J F Santana1, M Parida2, A Long3, J Birdsall3, K Rogers3, M Aguilera3, S McDermott3, and J R Manak1,2,3,4
1Interdisciplinary Graduate Program in Genetics, University of Iowa, Iowa City, IA.
2Interdisciplinary Graduate Program in Informatics, University of Iowa, Iowa City, IA.
3Department of Biology, University of Iowa, Iowa City, IA.
4Department of Pediatrics, University of Iowa Carver College of Medicine, Iowa City, IA.
c-Myb is a proto-oncogene which when mutated causes leukemia and lymphoma in birds and mammals. Vertebrates contain three representatives of the Myb gene family consisting of A-, B- and c-Myb, all of which encode DNA-binding factors that are important for the proper expression of large numbers of genes including those that regulate cell cycle progression. Drosophila melanogaster contains a single Myb gene (Dm-Myb), mutants of which die before reaching adulthood. Dm-Myb protein is present in a complex which includes the nucleosome remodeling factor NURF. Through yeast two-hybrid experiments and genetic screens, we have shown that Dm-Myb is directly interacting with the major subunit of NURF (NURF301). In light of these results, we performed gene expression analyses in wing discs of Dm-Myb and Nurf301 mutant animals and found that there is a strong overlap of the genes regulated by these two proteins. We show that in vivo, as previously reported in cell lines, Dm-Myb is necessary for the activation of cell cycle genes, specifically those involved in the G2/M transition. However, despite the strong overlap of genes co-regulated by Dm-Myb and NURF, the latter is not required for the regulation of this class of genes, suggesting that Dm-Myb and NURF function together in some contexts but independently in others. Consistent with these data, Dm-Myb, but not Nurf301, mutant wing discs have an increased mitotic index, with only Dm-Myb mutant animals showing a significant developmental delay presumably due to the increased time required for mitotic cells to progress through G2/M.