Transcriptional Profiling Of Myb Mutant Flies Reveals Ectopic Activation Of LTR-Retrotransposons

c-Myb is a proto-oncogene that belongs to a family of chromatin factors which share a conserved DNA-binding domain. Vertebrates have three representatives of this gene family consisting of A-, B- and c-Myb. Drosophila melanogaster contains a single Myb gene (Dm-Myb) most like B-Myb.  Although siRNA knockdown of Dm-Myb was shown to cause aberrant expression of genes with prominent roles in coordinating cell division in an embryonic Drosophila cell line (Kc cells), many other classes of genes were also affected.  Along the same lines, Dm-Myb mutant flies display cell cycle defects such as aneuploidy, polyploidy and abnormal centrosome number.  However, other than one report utilizing siRNA and tissue culture, no study has attempted an empirical analysis of global transcriptional changes occurring in Myb mutant animals. Thus, we have performed tiling microarray studies to empirically assess genome-wide transcription in salivary gland cells of wild type and Myb null larvae. Three differentially regulated classes of transcripts were identified: 1) genes that are targets of Myb in Kc cells but not in salivary glands, 2) genes that are targets of Myb in salivary glands but not in Kc cells and, 3) retrotransposons.  Interestingly, specific families of retrotransposons within different classes showed differential regulation. Non-LTR retrotransposons from the Jockey sub-family were downregulated while LTR-retrotransposons from the Pao sub-family were up-regulated. In conclusion, our studies demonstrate that Dm-Myb has different functions in different tissues, and in the absence of Myb, LTR-specific retrotransposons are upregulated, potentially contributing to the genomic instability observed in myb mutant animals.