(Here I went down a bit of a literature rabbit hole trying to understand how this could happen, but thanks to some great work in the trypanosome T. brucei, we hypothesize that the sub- and neofunctionalization of Dot1 homologs may be the key!) 7.5/n
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Dearest to me is the diversity of histone modification combinations found in repressed heterochromatin. Traditionally, constitutive heterochromatin on transposable elements was defined by H3K9 methylation, and facultative heterochromatin on silent genes was defined by H3K27me3. 8/n
My favourite example is from the chytrid fungus S. punctatus, which has a near perfect colocalization of H3K9me3 and H3K27me3 encompassing both TEs and genes (reminiscent of the effect of the dual writing ability of Ezl1 in ciliates) 10/n
We hypothesize that the evolutionary arms race between TEs and their repression (and co-option) by host genomes helps drive diversity. But a missing component is the readers of these histone modifications and their downstream interactors, which I aim to address during the rest of my postdoc! 11/n
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