DNA loop anchorage region colocalizes with the replication origin located downstream to the human gene encoding lamin B2

Lagarkova, Maria A.; Svetlova, Ekaterina; Giacca, Mauro; Falaschi, Arturo; Razin, Sergey V.

doi:10.1002/(sici)1097-4644(19980401)69:1<13::aid-jcb2>3.0.co;2-y

Cited by 35 publications

(23 citation statements)

References 17 publications

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“…A Nbs1-dependent checkpoint pathway could be involved in preventing origin firing by a cisacting mechanism (7). Although several points remain to be proved, a partial support to this model is provided by the observation that a Topo II-DNA complex maps adjacent to the Lamin B2 origin, which is activated in the first minute of the S phase (37).…”

Section: Discussionmentioning

confidence: 99%

The Dispersal of Replication Proteins after Etoposide Treatment Requires the Cooperation of Nbs1 with the Ataxia Telangiectasia Rad3-Related/Chk1 Pathway

et al. 2006

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In mammalian cells, DNA replication takes place in functional subnuclear compartments, called replication factories, where replicative factors accumulate. The distribution pattern of replication factories is diagnostic of the different moments (early, mid, and late) of the S phase. This dynamic organization is affected by different agents that induce cell cycle checkpoint activation via DNA damage or stalling of replication forks. Here, we explore the cell response to etoposide, an anticancer drug belonging to the topoisomerase II poisons. Etoposide does not induce an immediate block of DNA synthesis and progressively affects the distribution of replication proteins in S phase. First, it triggers the formation of large nuclear foci that contain the single-strand DNA binding protein replication protein A (RPA), suggesting that lesions produced by the drug are processed into extended singlestranded regions. These RPA foci colocalize with DNA replicated at the beginning of the treatment. Etoposide also triggers the dispersal of replicative proteins, proliferating cell nuclear antigen and DNA ligase I, from replication factories. This event requires the activity of the ataxia telangiectasia Rad3-related (ATR) checkpoint kinase. By comparing the effect of the drug in cell lines defective in different DNA repair and checkpoint pathways, we show that, along with the downstream kinase Chk1, the Nbs1 protein, mutated in the Nijmegen breakage syndrome, is also relevant for this response and for ATR-dependent phosphorylation. Finally, our analysis evidences a critical role of Nbs1 in the etoposideinduced inhibition of

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Section: Discussionmentioning

confidence: 99%

The Dispersal of Replication Proteins after Etoposide Treatment Requires the Cooperation of Nbs1 with the Ataxia Telangiectasia Rad3-Related/Chk1 Pathway

et al. 2006

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“…First, many MARs are associated with origins of DNA replication. Indeed, MARs have been found at or very close to the chicken lysozyme DNA replication origin (Phi and Straetling 1988), the DHFR origins β and β′ (Dijkwel and Hamlin 1988), the lamin B2 origin (Lagarkova et al 1998), and the c-myc origin (GirardReydet et al 2004). Interestingly, origins/MARs association is a conserved feature ).…”

Section: Higher Levels Of Chromatin Organizationmentioning

confidence: 99%

Programming DNA replication origins and chromosome organization

2010

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During each cell cycle, thousands of DNA replication origins are activated in each cell of a metazoan organism. Although they appear site-specific, their usage and organization are rather plastic. Moreover, no strict sequence specificity has been observed in contrast to bacterial or Saccharomyces cerevisiae DNA replication origins. Epigenetic regulation linked to chromatin structure, chromosome organization, and transcription has been suggested to explain how DNA replication origins are selected and recognized by replication initiation factors. In this paper, we review these epigenetic features and discuss how, during the previous mitosis, chromosomal architecture might prepare DNA replication origins for a new cell cycle.

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“…In addition, it is emerging that they can bring together proximal and distal cis-regulatory elements at the nuclear matrix and shield chromatin domains from the effects of flanking regulatory regions (Nabirochkin et al 1998;Eivazova et al 2007;Girod et al 2007). The mapping of MARs directly to or in the vicinity of several origins of replication suggests that they may also participate in DNA replication (Lagarkova et al 1998;Girard-Reydet et al 2004).…”

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confidence: 99%

Reconfiguration of genomic anchors upon transcriptional activation of the human major histocompatibility complex

et al. 2008

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The folding of chromatin into topologically constrained loop domains is essential for genomic function. We have identified genomic anchors that define the organization of chromatin loop domains across the human major histocompatibility complex (MHC). This locus contains critical genes for immunity and is associated with more diseases than any other region of the genome. Classical MHC genes are expressed in a cell type-specific pattern and can be induced by cytokines such as interferon-gamma (IFNG). Transcriptional activation of the MHC was associated with a reconfiguration of chromatin architecture resulting from the formation of additional genomic anchors. These findings suggest that the dynamic arrangement of genomic anchors and loops plays a role in transcriptional regulation.

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DNA loop anchorage region colocalizes with the replication origin located downstream to the human gene encoding lamin B2

Cited by 35 publications

References 17 publications

The Dispersal of Replication Proteins after Etoposide Treatment Requires the Cooperation of Nbs1 with the Ataxia Telangiectasia Rad3-Related/Chk1 Pathway

The Dispersal of Replication Proteins after Etoposide Treatment Requires the Cooperation of Nbs1 with the Ataxia Telangiectasia Rad3-Related/Chk1 Pathway

Programming DNA replication origins and chromosome organization

Reconfiguration of genomic anchors upon transcriptional activation of the human major histocompatibility complex

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