Crystal Structure of the Human SUV39H1 Chromodomain and Its Recognition of Histone H3K9me2/3

Wang, Tao; Xu, Chao; Liu, Yanli; Fan, Kai; Li, Zhihong; Sun, Xingming; Ouyang, Hui; Zhang, Xuecheng; Zhang, Jiahai; Li, Yanjun; Mackenzie, F.; Min, Jinrong; Tu, Xiaoming

doi:10.1371/journal.pone.0052977

Cited by 59 publications

(55 citation statements)

References 39 publications

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“…However, recent Clr4 studies in fission yeast demonstrated that not only Swi6 CD but also Clr4 CD showed higher affinity for H3K9 methylation, and this interaction seemed to be crucial for Clr4 accumulation and H3K9me2/3 formation on heterochromatin (33). Furthermore and most recently, it has been reported that Suv39h CD also showed higher affinity to methylated H3K9 (highest to H3K9me3) in vitro (34). Therefore, our new findings and recent information strongly suggest that H3K9me3 deposited by Suv39h can directly tether its own enzyme to pericentric regions.…”

Section: Hp1 Binding To Suv39h1 Was Dispensable For the Establishmentmentioning

confidence: 99%

Pericentric Heterochromatin Generated by HP1 Protein Interaction-defective Histone Methyltransferase Suv39h1

Muramatsu

Singh

Kimurâ

et al. 2013

Journal of Biological Chemistry

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Background: Histone H3 lysine 9 trimethylation (H3K9me3) and heterochromatin protein HP1 accumulations are hallmarks of heterochromatin. Results: Pericentric accumulation of histone methyltransferase, Suv39h, and Suv39h-mediated H3K9me3 occurs without Suv39h-HP1 binding and HP1 accumulation. Conclusion:The functional relationship between Suv39h and HP1 for pericentric heterochromatin formation is clarified. Significance: The Suv39h-mediated heterochromatin formation can be further elucidated from this model.

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Section: Hp1 Binding To Suv39h1 Was Dispensable For the Establishmentmentioning

confidence: 99%

Pericentric Heterochromatin Generated by HP1 Protein Interaction-defective Histone Methyltransferase Suv39h1

Muramatsu

Singh

Kimurâ

et al. 2013

Journal of Biological Chemistry

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“…Therefore, it is possible that Suv39h1 also possesses RNA-binding activity, and nascent transcript is involved in creating Suv39h1's target specificity. In addition, it is already known that Suv39h1 CD possesses higher binding affinities for H3K9me2/3 (Wang et al, 2012). In Suv39h DKO cells, pericentric H3K9me3 is severely diminished, but global H3K9me3 is still heavily maintained by other H3K9 methyltransferases (Bulut-Karslioglu et al, 2014).…”

Section: Discussionmentioning

confidence: 99%

Pericentric H3K9me3 Formation by HP1 Interaction-defective Histone Methyltransferase Suv39h1

Muramatsu

Kimurâ

Kotoshiba³

et al. 2016

Cell Struct. Funct.

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ABSTRACT. Pericentric regions form epigenetically organized, silent heterochromatin structures that accumulate histone H3 lysine 9 tri-methylation (H3K9me3) and heterochromatin protein 1 (HP1), a methylated H3K9-binding protein. At pericentric regions, Suv39h is the major enzyme that generates H3K9me3. Suv39h also interacts directly with HP1. However, the importance of HP1 interaction for Suv39h-mediated H3K9me3 formation at the pericentromere is not well characterized. To address this question, we introduced HP1 bindingdefective, N-terminally truncated mouse Suv39h1 (ΔN) into Suv39h-deficient cells. Pericentric H3K9me3-positive cells were not detected by endogenous-level expression of ΔN. Notably, ΔN could induce pericentric accumulation of H3K9me3 as wild type Suv39h1 did if it was overexpressed. These findings demonstrate that the N-terminal region of Suv39h1, presumably via HP1-Suv39h1 interaction, is required for Suv39h1-mediated pericentric H3K9me3 formation, but can be overridden if Suv39h1 is overproduced, indicating that Suv39h1-mediated heterochromatin formation is controlled by multiple modules, including HP1.

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“…This accumulation was considered indirect and mediated by HP1 [52,53]. But SUV39H1 has also been shown self-sufficient for H3K9me3 binding in vitro [54] and in vivo [49,55,44], which is expected in principle since SUV39H1/2, like HP1, have a chromodomain. The partial disruption of heterochromatin by hyperacetylation using Trichostatin A (TSA) treatment, leads to the complete dislocation of HP1 from the residual chromocenters, whereas SUV39H1 still binds them [5].…”

Section: Chromocenter Formation and Suv39h1-hp1 Functional Relationshipsmentioning

confidence: 99%

A model of dynamic stability of H3K9me3 heterochromatin to explain the resistance to reprogramming of differentiated cells

Jehanno

Flouriot

Goff

et al. 2017

Biochimica et Biophysica Acta (BBA) - Gene Regulatory Mechanism

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Despite their dynamic nature, certain chromatin marks must be maintained over the long term. This is particulary true for histone 3 lysine 9 (H3K9) trimethylation, that is involved in the maintenance of healthy differentiated cellular states by preventing inappropriate gene expression, and has been recently identified as the most efficient barrier to cellular reprogramming in nuclear transfer experiments. We propose that the capacity of the enzymes SUV39H1/2 to rebind to a minor fraction of their products, either directly or via HP1α/β, contributes to the solidity of this mark through (i) a positive feedback involved in its establishment by the mutual enforcement of H3K9me3 and SUV39H1/2 and then (ii) a negative feedback sufficient to strongly stabilize H3K9me3 heterochromatin in post-mitotic cells by generating local enzyme concentrations capable of counteracting transient bursts of demethylation. This model does not require direct molecular interactions with adjacent nucleosomes and is favoured by a series of additional mechanisms including (i) the protection of chromatinbound SUV39H1/2 from the turnovers of soluble proteins, which can explain the uncoupling between the cellular contents in SUV39H1 mRNA and protein; (ii) the cooperative dependence on the local density of the H3K9me3 of HP1α/β-dependent heterochomatin condensation and, dispensably (iii) restricted enzyme exchanges with chromocenters confining the reactive bursts of SUV39H1/2 in heterochromatin. This mechanism illustrates how seemingly static epigenetic states can be firmly maintained by dynamic and reversible modifications.

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Crystal Structure of the Human SUV39H1 Chromodomain and Its Recognition of Histone H3K9me2/3

Cited by 59 publications

References 39 publications

Pericentric Heterochromatin Generated by HP1 Protein Interaction-defective Histone Methyltransferase Suv39h1

Pericentric Heterochromatin Generated by HP1 Protein Interaction-defective Histone Methyltransferase Suv39h1

Pericentric H3K9me3 Formation by HP1 Interaction-defective Histone Methyltransferase Suv39h1

A model of dynamic stability of H3K9me3 heterochromatin to explain the resistance to reprogramming of differentiated cells

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