Facultative Heterochromatin Lab Report
Introduction/Background c-Myb has long been known as a factor of many leukemias and lymphomas in mammals and birds. Vertebrates possess 3 forms of the Myb gene, A-Myb, B-Myb, and c-Myb, whereas Drosophila melanogaster, however, only possess one copy of the Myb gene, Dm-Myb, which results in fatality before reaching adulthood (Manak, Mikitu, Lipsick, 2002). Myb has also been shown to be required for the proper activation of G2/M cell cycle genes (Georlette et al., 2007). The results of several other experiments lead our lab to suspect that Myb is involved in facultative heterochromatin stabilization. Chromatin, made up of DNA and associated proteins, can be euchromatic or heterochromatic; euchromatin is mainly associated with active transcription, whereas heterochromatin is associated with repressed transcription. Active euchromatin and repressive heterochromatin are established by post-translational marks such as methyl groups placed on the histone around which DNA is wrapped. Histone 3 lysine 4 is methylated to promote active transcription, whereas histone 3 lysine 27 is methylated to promote the formation of facultative heterochromatin (which is associated with
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This may be due to the fact that Pc3 encodes a more severe antimorphic protein that makes the animal more susceptible to relevant genetic interactors. Identification of a genetic interaction between Myb and Pc is consistent with Myb’s role in stabilizing H3K27me3, the histone mark associated with facultative heterochromatin which is the mark that is bound by Pc. We also observed a complete lack of GFP negative larvae in the Ash1 crosses, indicating a particularly strong genetic interaction between Myb and either of two Ash1 alleles. This may be due to Myb’s vital role in activation of transcription for hundreds of target
This may be due to the fact that Pc3 encodes a more severe antimorphic protein that makes the animal more susceptible to relevant genetic interactors. Identification of a genetic interaction between Myb and Pc is consistent with Myb’s role in stabilizing H3K27me3, the histone mark associated with facultative heterochromatin which is the mark that is bound by Pc. We also observed a complete lack of GFP negative larvae in the Ash1 crosses, indicating a particularly strong genetic interaction between Myb and either of two Ash1 alleles. This may be due to Myb’s vital role in activation of transcription for hundreds of target