The effects of SUUR protein suggest its role in repressive chromatin renewal during replication in<i>Drosophila</i>

Posukh, Olga V.; Maksimov, Daniil A.; Skvortsova, Ksenia; Koryakov, Dmitry E.; Belyakin, Stepan N.

doi:10.1080/19491034.2015.1074366

Cited by 9 publications

(14 citation statements)

References 23 publications

(33 reference statements)

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“…The bacterial terminus, bracketed by the inverted termination sites, is a well-known system to ensure that replication is unidirectional through most of the prokaryotic circular chromosome, but do similar developmental stage-specific systems maintain region-specific over-replicons in the polytene chromosomes of eukaryotes? The SuUR protein in Drosophila may be a component of one such system [ 25 , 46 ]. There also has to be a general system that controls spreading along the chromosome of onion-skin replication initiated from randomly inserted mobile elements.…”

Section: Discussionmentioning

confidence: 99%

“…At least two phenomena contribute to heterochromatin underreplication at the genome level [ 41 ]: (1) active suppression of the replication initiation in heterochromatin and (2) replication fork stalling at the heterochromatin boundaries. The protein complex responsible for sRFs at the heterochromatin boundaries in Drosophila , whose name "suppressor of underreplication" (SuUR) reflects the phenotype of the corresponding mutant [ 44 , 45 ], regulates heterochromatin-specific histone modification [ 46 ]. Thus, "underreplication" is another code name for elevated CRC.…”

Section: Underreplicationmentioning

confidence: 99%

“…As an interesting, simpler variation of this arrangement, if there are multiple firings of a replication origin between the closest pair of termination sites, the replified structure becomes unstable in this case, as multiple replication forks rear-end into the original forks blocked at the termination sites, forming linear DNA fragments spanning the chromosomal segment between the termination sites ( Fig 4C , right, a schematic presentation of Fig 2B ). The scenario analogous to unstable nested bubbles is observed in the underreplicated heterochromatic regions of polytene chromosomes [ 25 , 46 , 78 ].…”

Section: Amplification Versus Replificationmentioning

confidence: 99%

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Chromosomal Replication Complexity: A Novel DNA Metrics and Genome Instability Factor

Kuzminov

2016

PLoS Genet

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As the ratio of the copy number of the most replicated to the unreplicated regions in the same chromosome, the definition of chromosomal replication complexity (CRC) appears to leave little room for variation, being either two during S-phase or one otherwise. However, bacteria dividing faster than they replicate their chromosome spike CRC to four and even eight. A recent experimental inquiry about the limits of CRC in Escherichia coli revealed two major reasons to avoid elevating it further: (i) increased chromosomal fragmentation and (ii) complications with subsequent double-strand break repair. Remarkably, examples of stable elevated CRC in eukaryotic chromosomes are well known under various terms like "differential replication," "underreplication," "DNA puffs," "onion-skin replication," or "re-replication" and highlight the phenomenon of static replication fork (sRF). To accurately describe the resulting "amplification by overinitiation," I propose a new term: "replification" (subchromosomal overreplication). In both prokaryotes and eukaryotes, replification, via sRF processing, causes double-strand DNA breaks and, with their repair elevating chromosomal rearrangements, represents a novel genome instability factor. I suggest how static replication bubbles could be stabilized and speculate that some tandem duplications represent such persistent static bubbles. Moreover, I propose how static replication bubbles could be transformed into tandem duplications, double minutes, or inverted triplications. Possible experimental tests of these models are discussed.

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Section: Discussionmentioning

confidence: 99%

Section: Underreplicationmentioning

confidence: 99%

Section: Amplification Versus Replificationmentioning

confidence: 99%

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Chromosomal Replication Complexity: A Novel DNA Metrics and Genome Instability Factor

Kuzminov

2016

PLoS Genet

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“…O.V. Posukh et al (2015) suggests that the SUUR-dependent replication delay is important for a proper post-replication chromatin assembly. The SuUR mutation changes levels of H3K27me3 and H3K9me3 in late replicating regions of polytene chromosomes of salivary glands and pseudonurse cells of otu 11 mutants (Koryakov et al, 2011;Sher et al, 2012;Posukh et al, 2017).…”

Section: Distinct Properties Of Replication In Drosophila Polytene Chmentioning

confidence: 99%

“…According to O.V. Posukh et al (2017), SUUR in Drosophila chromosomes is involved in the epigenetic inheritance of H3K27me3 in those regions where Polycomb complexes only establish, but do not maintain H3K27me3 silencing (Posukh et al, 2015(Posukh et al, , 2017.…”

Section: Distinct Properties Of Replication In Drosophila Polytene Chmentioning

confidence: 99%

Replication timing in Drosophila and its peculiarities in polytene chromosomes

2019

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Drosophila melanogaster is one of the popular model organisms in DNA replication studies. Since the 1960s, DNA replication of polytene chromosomes has been extensively studied by cytological methods. In the recent two decades, the progress in our understanding of DNA replication was associated with new techniques. Use of fluorescent dyes increased the resolution of cytological methods significantly. High-throughput methods allowed analysis of DNA replication on a genome scale, as well as its correlation with chromatin structure and gene activi ty. Precise mapping of the cytological structures of polytene chromosomes to the genome assembly allowed comparison of replication between polytene chromosomes and chromosomes of diploid cells. New features of replication characteristic for D. melanogaster were described for both diploid and polytene chromosomes. Comparison of genomic replication profiles revealed a significant similarity between Drosophila and other well-studi ed eukaryotic species, such as human. Early replication is often confined to intensely transcribed gene-dense regions characterized by multiple replication initiation sites. Features of DNA replication in Drosophila might be explained by a compact genome. The organization of replication in polytene chromosomes has much in common with the organization of replication in chromosomes in diploid cells. The most important feature of replication in polytene chromosomes is its low rate and the dependence of S-phase duration on many factors: external and internal, local and global. The speed of replication forks in D. melanogaster polytene chromosomes is affected by SUUR and Rif1 proteins. It is not known yet how universal the mechanisms associated with these factors are, but their study is very promising.

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Drosophila SUMM4 complex couples insulator function and DNA replication timing control

Andreyeva

Emelyanov

Nevil³

et al. 2021

Preprint

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The asynchronous timing of replication of different chromosome domains is essential for eukaryotic genome stability, but the mechanisms establishing replication timing programs remain incompletely understood. Drosophila SNF2-related factor SUUR imparts under-replication (UR) of late-replicating intercalary heterochromatin (IH) domains in polytene chromosomes1. SUUR negatively regulates DNA replication fork progression across IH; however, its mechanism of action remains obscure2,3. Here we developed a novel method termed MS-Enabled Rapid protein Complex Identification (MERCI) to isolate a stable stoichiometric native complex SUMM4 that comprises SUUR and a chromatin boundary protein Mod(Mdg4)-67.24,5. In vitro, Mod(Mdg4) stimulates the ATPase activity of SUUR, although neither SUUR nor SUMM4 can remodel nucleosomes. Mod(Mdg4)-67.2 and SUUR distribution patterns in vivo partially overlap, and Mod(Mdg4) is required for a normal spatiotemporal distribution of SUUR in chromosomes. SUUR and Mod(Mdg4)-67.2 mediate insulator activities of the gypsy mobile element that disrupt enhancer-promoter interactions and establish euchromatin-heterochromatin barriers in the genome. Furthermore, mutations of SuUR or mod(mdg4) reverse the locus-specific UR. These findings reveal that DNA replication can be delayed by a chromatin barrier and thus, uncover a critical role for architectural proteins in replication timing control. They also provide a biochemical link between ATP-dependent motor factors and the activity of insulators in regulation of gene expression and chromatin partitioning.

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The effects of SUUR protein suggest its role in repressive chromatin renewal during replication inDrosophila

Cited by 9 publications

References 23 publications

Chromosomal Replication Complexity: A Novel DNA Metrics and Genome Instability Factor

Chromosomal Replication Complexity: A Novel DNA Metrics and Genome Instability Factor

Replication timing in Drosophila and its peculiarities in polytene chromosomes

Drosophila SUMM4 complex couples insulator function and DNA replication timing control

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