Methylation of H3K4 Is Required for Inheritance of Active Transcriptional States

Muramoto, Tetsuya; Müller, Iris; Thomas, Giles; Melvin, Andrew; Chubb, Jonathan R.

doi:10.1016/j.cub.2010.01.017

Cited by 169 publications

(181 citation statements)

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“…SET1 Deletion Causes Increased CTD Serine 5 Phosphorylation-Although cells lacking SET1 exhibit changes in the transcription levels of some genes (12,37), they often show alterations in the induction or repression kinetics of regulated genes (13,38,39). Deletion of SET1 also confers sensitivity to the drug 6AU (20), which slows transcription elongation by depleting NTP pools.…”

Section: Resultsmentioning

confidence: 99%

Yeast Swd2 Is Essential Because of Antagonism between Set1 Histone Methyltransferase Complex and APT (Associated with Pta1) Termination Factor

Soares¹,

Buratowski

2012

Journal of Biological Chemistry

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Section: Resultsmentioning

confidence: 99%

Yeast Swd2 Is Essential Because of Antagonism between Set1 Histone Methyltransferase Complex and APT (Associated with Pta1) Termination Factor

Soares¹,

Buratowski

2012

Journal of Biological Chemistry

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“…In mammals, the TrxG MLL proteins (see Box 1) bind mitotic chromatin (Blobel et al, 2009). Furthermore, experiments in Xenopus and in Dictyostelium discoideum indicate a requirement for methylation of the H3K4 residue itself in mediating epigenetic memory of transcriptional activity during mitosis: when the K4 residue of histone H3 is mutated to glutamate (Ng and Gurdon, 2008) or alanine (Muramoto et al, 2010), epigenetic memory of transcriptional activity across mitotic divisions is disrupted. PcG complexes also remain associated with mitotic chromosomes, although to a lesser extent than Trithorax, and they co-localize with H3K27me3 on metaphase chromosomes in mammalian cells (Vincenz and Kerppola, 2008;Follmer et al, 2012;Fonseca et al, 2012).…”

Section: Proposed Role 3: Poising For Totipotency and Preparing For Rmentioning

confidence: 99%

Poised chromatin in the mammalian germ line

Lesch

Page

2014

Development

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Poised (bivalent) chromatin is defined by the simultaneous presence of histone modifications associated with both gene activation and repression. This epigenetic feature was first observed at promoters of lineage-specific regulatory genes in embryonic stem cells in culture.More recent work has shown that, in vivo, mammalian germ cells maintain poised chromatin at promoters of many genes that regulate somatic development, and that they retain this state from fetal stages through meiosis and gametogenesis. We hypothesize that the poised chromatin state is essential for germ cell identity and function. We propose three roles for poised chromatin in the mammalian germ line: prevention of DNA methylation, maintenance of germ cell identity and preparation for totipotency. We discuss these roles in the context of recently proposed models for germline potency and epigenetic inheritance.

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“…H3K4 methylation is retained on mitotic chromatin in S. pombe, Dictyostelium, and human cells (Noma and Grewal 2002;Muramoto et al 2010), suggesting that this epigenetic mark might be involved in the regulation of chromatin through Figure 6 The absence of Set1 complex function in combination with partial NIMA function results in enhanced mitotic delays. (A) The time spent in the first mitosis by each of the mutant strains is indicated compared to the WT strain.…”

Section: Set1 Complex Function Is Required With Nima For Normal Transmentioning

confidence: 99%

“…Alternatively, since our data show that Set1 complex function is required along with mitotic CDK1 to promote mitosis, absence of An-swd1 function alone might cause defects in the G2-M transition that are not manifested when NIMA and CDK1 are fully functional. However when cells lacking An-swd1 undergo mitosis in the absence of sufficient NIMA (nimA7 + An-swd1 at 35°), downstream defects in mitosis may be triggered because of the G2-M transition defects caused by lack of Set1 complex function.H3K4 methylation is retained on mitotic chromatin in S. pombe, Dictyostelium, and human cells (Noma and Grewal 2002;Muramoto et al 2010), suggesting that this epigenetic mark might be involved in the regulation of chromatin through Figure 6 The absence of Set1 complex function in combination with partial NIMA function results in enhanced mitotic delays. (A) The time spent in the first mitosis by each of the mutant strains is indicated compared to the WT strain.…”

mentioning

confidence: 99%

“…Moreover, in human cells, methylated H3K4 has been proposed to mark the site for the return of transcription factors to target genes at the end of mitosis (Kelly et al 2010). In addition, H3K4 methylation has been implicated not in determining the level of transcription, but the inheritance of transcription states from the mother cell to daughter Dictyostelium cells (Muramoto et al 2010;Peterson 2010). Therefore, another potential explanation for the enhanced mitotic defects in nimA7 + DAn-swd1 cells is that the Set1 complex is required to mediate the resetting of gene expression to an interphase-like state after mitosis.…”

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confidence: 99%

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The Set1/COMPASS Histone H3 Methyltransferase Helps Regulate Mitosis With the CDK1 and NIMA Mitotic Kinases in Aspergillus nidulans

et al. 2014

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Mitosis is promoted and regulated by reversible protein phosphorylation catalyzed by the essential NIMA and CDK1 kinases in the model filamentous fungus Aspergillus nidulans. Protein methylation mediated by the Set1/COMPASS methyltransferase complex has also been shown to regulate mitosis in budding yeast with the Aurora mitotic kinase. We uncover a genetic interaction between An-swd1, which encodes a subunit of the Set1 protein methyltransferase complex, with NIMA as partial inactivation of nimA is poorly tolerated in the absence of swd1. This genetic interaction is additionally seen without the Set1 methyltransferase catalytic subunit. Importantly partial inactivation of NIMT, a mitotic activator of the CDK1 kinase, also causes lethality in the absence of Set1 function, revealing a functional relationship between the Set1 complex and two pivotal mitotic kinases. The main target for Set1-mediated methylation is histone H3K4. Mutational analysis of histone H3 revealed that modifying the H3K4 target residue of Set1 methyltransferase activity phenocopied the lethality seen when either NIMA or CDK1 are partially functional. We probed the mechanistic basis of these genetic interactions and find that the Set1 complex performs functions with CDK1 for initiating mitosis and with NIMA during progression through mitosis. The studies uncover a joint requirement for the Set1 methyltransferase complex with the CDK1 and NIMA kinases for successful mitosis. The findings extend the roles of the Set1 complex to include the initiation of mitosis with CDK1 and mitotic progression with NIMA in addition to its previously identified interactions with Aurora and type 1 phosphatase in budding yeast.D URING the transition from interphase into mitosis, chromatin undergoes dramatic global restructuring to go from a relaxed interphase configuration amenable to gene expression to a condensed form characteristic of mitotic chromosomes. Chromatin condensation not only marks mitosis but is also essential for the normal segregation of the duplicated sister chromatids into daughter nuclei. On the other hand, during mitotic exit, decondensation of chromatin needs to be triggered in a correct temporal manner to enable successful transition into interphase. In Aspergillus nidulans, a model filamentous fungus that enabled discovery of cell cycle-specific genes, mitotic initiation requires the function of the essential NIMA mitotic kinase (Oakley and Morris 1983;Osmani et al. 1987). Early evidence pointed to a role for NIMA in regulating chromatin compaction through the cell cycle since overexpression of NIMA was sufficient to induce chromatin condensation independent of cell cycle phase (Osmani et al. 1988;. Importantly, NIMA is required for, and can promote, the phosphorylation of histone H3 at serine 10 (De Souza et al. 2000), a universal marker of mitotic chromatin. In addition, NIMA has been shown to regulate the partial disassembly of nuclear pore complexes, allowing the access of mitotic regulators to the nucleus (Wu et al. 1998;De S...

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Methylation of H3K4 Is Required for Inheritance of Active Transcriptional States

Abstract: Our data indicate that methylated H3K4 can act as a chromatin mark reflecting the original meaning of "epigenetic."

Cited by 169 publications

References 54 publications

Yeast Swd2 Is Essential Because of Antagonism between Set1 Histone Methyltransferase Complex and APT (Associated with Pta1) Termination Factor

Yeast Swd2 Is Essential Because of Antagonism between Set1 Histone Methyltransferase Complex and APT (Associated with Pta1) Termination Factor

Poised chromatin in the mammalian germ line

The Set1/COMPASS Histone H3 Methyltransferase Helps Regulate Mitosis With the CDK1 and NIMA Mitotic Kinases in Aspergillus nidulans

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