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. Author manuscript; available in PMC: 2012 Apr 8.
Published in final edited form as: Mol Cell. 2011 Apr 8;42(1):118–126. doi: 10.1016/j.molcel.2011.03.006

Figure 5. Histone H3K79 residue is required for proper mating type silencing, but Dot1 and H3K79 methylation does not play a role in this process.

Figure 5

Wild-type, dot1Δ, sir3Δ, or H3K79A strains were plated on YPD and tested for growth inhibition in the presence of the indicated concentration of alpha factor in a halo assay test. Both sir3Δ and H3K79A mutants were resistant to alpha factor arrest. However, strains lacking H3K79 methylation due to deletion of DOT1 are inhibited to a similar extent as the wild-type strain. This indicates that H3K79 methylation in itself is not required for proper HML silencing.