Keeping chromatin quiet

Mermoud, Jacqueline E.; Rowbotham, Samuel P.; Varga‐Weisz, Patrick

doi:10.4161/cc.10.23.18558

Cited by 29 publications

(20 citation statements)

References 93 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…102 SMARCAD1 is brought to replicating regions via direct interaction with the replicative clamp, PCNA, where it deacetylates the newly deposited H3 and H4 histones (Fig. 2c).…”

Section: Remodeling Complexes That Establish or Remove Histone Marksmentioning

confidence: 99%

Chromatin dynamics: Interplay between remodeling enzymes and histone modifications

Swygert

Peterson

2014

Biochimica et Biophysica Acta (BBA) - Gene Regulatory Mechanism

206

148

View full text Add to dashboard Cite

Chromatin dynamics play an essential role in regulating the accessibility of genomic DNA for a variety of nuclear processes, including gene transcription and DNA repair. The posttranslational modification of the core histones and the action of ATP-dependent chromatin remodeling enzymes represent two primary mechanisms by which chromatin dynamics are controlled and linked to nuclear events. Although there are examples in which a histone modification or a remodeling enzyme may be sufficient to drive a chromatin transition, these mechanisms typically work in concert to integrate regulatory inputs, leading to a coordinated alteration in chromatin structure and function. Indeed, site-specific histone modifications can facilitate the recruitment of chromatin remodeling enzymes to particular genomic regions, or they can regulate the efficiency or the outcome of a chromatin remodeling reaction. Conversely, chromatin remodeling enzymes can also influence, and sometimes directly modulate, the modification state of histones. These functional interactions are generally complex, frequently transient, and often require the association of myriad additional factors.

show abstract

“…102 SMARCAD1 is brought to replicating regions via direct interaction with the replicative clamp, PCNA, where it deacetylates the newly deposited H3 and H4 histones (Fig. 2c).…”

Section: Remodeling Complexes That Establish or Remove Histone Marksmentioning

confidence: 99%

Chromatin dynamics: Interplay between remodeling enzymes and histone modifications

Swygert

Peterson

2014

Biochimica et Biophysica Acta (BBA) - Gene Regulatory Mechanism

206

148

View full text Add to dashboard Cite

show abstract

“…Among the putative genes whose depletion has a significant impact is CENP-C, which was previously found to stabilize CENP-A (Falk et al, 2015) and served as a control in our screen. In addition we find groups of genes involved particularly in 1) SUMO/Ubiquitin transactions, such as SENP6, a SUMO protease (Mukhopadhyay and Dasso, 2007), 2) chromatin remodelers that include SMARCAD1, a SWI/SNF type chromatin remodeler involved in chromatin reconstitution following DNA replication (Taneja et al, 2017;Mermoud et al, 2011), 3) chromatin modifiers such as SETD2 a H3K36 histone methyltransferase (Edmunds et al, 2008;Yuan et al, 2009), 4) factors involved in transcription regulation, notably NACC2, a POZ domain containing protein (Xuan et al, 2013) and also 5) DNA replication and repair factors such as the DNA mismatch repair protein PMS2 (Kolodner and Marsischky, 1999). See pathway-clustered groups of genes in table 1.…”

Section: Genetic Screening Identifies Novel Cenp-a Assembly and Maintmentioning

confidence: 94%

“…Among these we found known assembly factors including the CENP-A specific chaperone HJURP and all members of the Mis18 complex, M18BP1, Mis18α and M18β as well as CENP-C. Further we identified several novel components not previously associated with CENP-A assembly. Among DNA replication and repair factors we find MCM3 (Alabert and Groth, 2012) and POLD2 as well as the chromatin remodeler SMARCAD1 (Mermoud et al, 2011) and the transcription regulator CBX7, a Polycomb repressive complex 1 (PRC1) member (Blackledge et al, 2015). See pathway-clustered groups of genes in tables 1, 2, S2 and S3 and further description of the candidate factors in the discussion.…”

Section: Genetic Screening Identifies Novel Cenp-a Assembly and Maintmentioning

confidence: 99%

Genetic screening identifies a SUMO protease dynamically maintaining centromeric chromatin and the associated centromere complex

Mitra

Bodor

David

et al. 2019

Preprint

View full text Add to dashboard Cite

Centromeres are defined by a unique self-propagating chromatin structure featuring nucleosomes containing the histone H3 variant CENP-A. CENP-A turns over slower than general chromatin and a key question is whether this unusual stability is intrinsic to CENP-A nucleosomes or rather imposed by external factors. We designed a specific genetic screen to identify proteins involved in CENP-A stability based on SNAP-tag pulse chase labeling. Using a double pulse-labeling approach we simultaneously assay for factors with selective roles in CENP-A chromatin assembly. We discover a series of new proteins involved in CENP-A propagation, including proteins with known roles in DNA replication, repair and chromatin modification and transcription, revealing that a broad set of chromatin regulators impacts in CENP-A transmission through the cell cycle.The key factor we find to strongly affect CENP-A stability is SENP6. This SUMO-protease controls not only the levels of chromatin bound CENP-A but is required for the maintenance of virtually the entire centromere and kinetochore, with the exception of CENP-B. Acute depletion of SENP6 protein reveals its requirement for maintaining centromeric CENP-A levels throughout the cell cycle, suggesting that a dynamic SUMO cycle underlies a continuous surveillance of the centromere complex.

show abstract

“…Additionally, it interacts with HP1 and subsequently with SETDB1 [5,10], histone deacetylase 1 (HDAC1) and histone deacetylase 2 (HDAC2), and the nucleosome-remodeling factor CHD3 isoform 1 (CHD3.1) [11]. SMARCAD1 acts at replication sites to facilitate the deacetylation of newly assembled histones and thus acts to maintain correct silencing [12]. It has also been proposed to weaken histone–DNA interactions in nucleosomes flanking DSBs, facilitating the resection of DNA at DSBs in preparation for homologous recombination (HR) [13].…”

Section: The Structure Importance and Maintenance Of Heterochromatinmentioning

confidence: 99%

Repair of DNA Double-Strand Breaks in Heterochromatin

Watts

2016

Biomolecules

View full text Add to dashboard Cite

DNA double-strand breaks (DSBs) are among the most damaging lesions in DNA, since, if not identified and repaired, they can lead to insertions, deletions or chromosomal rearrangements. DSBs can be in the form of simple or complex breaks, and may be repaired by one of a number of processes, the nature of which depends on the complexity of the break or the position of the break within the chromatin. In eukaryotic cells, nuclear DNA is maintained as either euchromatin (EC) which is loosely packed, or in a denser form, much of which is heterochromatin (HC). Due to the less accessible nature of the DNA in HC as compared to that in EC, repair of damage in HC is not as straightforward as repair in EC. Here we review the literature on how cells deal with DSBs in HC.

show abstract

Keeping chromatin quiet

Cited by 29 publications

References 93 publications

Chromatin dynamics: Interplay between remodeling enzymes and histone modifications

Chromatin dynamics: Interplay between remodeling enzymes and histone modifications

Genetic screening identifies a SUMO protease dynamically maintaining centromeric chromatin and the associated centromere complex

Repair of DNA Double-Strand Breaks in Heterochromatin

Contact Info

Product

Resources

About