ctrometry and dual modification H3K9me3S10ph-specific antibodies. Indeed, phosphorylation of H3S10 in Acacetin chemical information mitosis displaces HP1 proteins bound to the adjacent H3K9me3. Similarly, cooccurrence of H3T3ph and H3K4me3 is supported by a recent study, which used combinatorial modification-specific antibodies to show that phosphorylated H3T3 is in cis to H3K4me3. These findings indicate that H3K4me3 and H3T3ph modifications can coexist on a single H3 molecule during mitosis. TFIID and PubMed ID:http://www.ncbi.nlm.nih.gov/pubmed/19828691 mitosis TFIID association with mitotic chromatin has been addressed previously by cell biological and biochemical experiments. & 2010 European Molecular Biology Organization Immunofluorescence staining and a limited ChIP study indicated that majority of TFIID leaves the condensed mitotic chromatin, although chromatin fractionation and other ChIP experiments indicated that at least some TFIID remains associated with chromatin during mitosis. It is interesting to note that the promoters analysed by ChIP in these studies all contained the canonical TATA sequence. In this context, it is also interesting that MLL association with mitotic chromatin and persistence of the H3K4me3 mark has been proposed to facilitate inheritance of active gene expression states during cell division. In our experiments, exclusion of TAF5 from the metaphase plate and anaphase chromosomes is clearly evident both in immunofluorescence of fixed cells and by live-cell imaging of GFP-tagged TAF5, but it is possible that a minor population of TFIID remains bound to mitotic chromatin. We speculate that H3T3 phosphorylation is delayed by the H3K4me3 mark, consistent with the reduced haspin activity observed on H3K4me3-containing peptide. This suggests a model in which the methylation state of the adjacent H3K4 residue has a function in the timing of depletion of PHD proteins from mitotic chromosomes. H3T3ph may be involved in displacement of a variety of proteins in mitosis. Perhaps the graded inhibitory effect of H3K4 methylation regulates H3T3ph deposition on chromatin so that 
it will first displace proteins that do not require H3K4me3 for binding, before dislodging H3K4me3-binding proteins. High densities of H3K4me3 or strong core promoter binding may allow retention of TFIID at specific promoters. Such a mechanism could also serve to ensure that haspin displaces TFIID only in mitosis when its activity is high, and not in interphase. This principle could be relevant to regulation of other lysine-methylation switches. Our combined results show that H3T3 phosphorylation by the mitotic haspin kinase has a negative effect on the transcription function of TAF3 and on the association of TFIID to mitotic chromosomes. This suggests that a `phosphomethyl’ switch involving H3T3 and H3K4 is relevant for the interaction of TFIID to chromatin. In case of TFIID, this switch may serve to allow a rapid reassociation of TFIID to H3K4me3-marked chromatin after chromosome segregation. Indeed, we observe a rapid association of TFIID during late anaphase, which occurs well before chromosome decondensation. We propose that this correlates with removal of the H3T3ph mark by the action of yet-to-be identified protein phosphatases. Taken together, our experiments identify a new `phospho methyl’ switch involving the haspin kinase and the PHD of TAF3 in regulating TFIID activity and chromatin association. Our results also highlight the importance of crosstalk between histone modifications during mitotic progression of the ce