Rearrangement of mammalian chromatin structure following excision repair

Zolan, Miriam E.; Smith, Charles A.; Calvin, Noel M.; Hanawalt, Philip C.

doi:10.1038/299462a0

Cited by 48 publications

(14 citation statements)

References 21 publications

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“…In addition, UVC-damaged chromatin decondensation was confirmed by cytological observations that were based on analyses of prematurely condensed chromosomes [21]. Remarkably, the increased nuclease sensitivity of damaged regions was independent of the initial distribution of UV photoproducts in chromatin [22], further supporting a chromatin unfolding model rather than NER occurring preferentially in accessible chromatin regions. Altogether, these studies set the first principles of the Unfolding-Refolding model that describes the transitions in chromatin structure during NER, with first chromatin unfolding then followed by refolding of newly repaired DNA into nucleosomes (Fig.…”

Section: Emergence Of the Arr Model: From The Original Concepts To A mentioning

confidence: 88%

Chromatin dynamics after DNA damage: The legacy of the access–repair–restore model

2015

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Eukaryotic genomes are packaged into chromatin, which is the physiological substrate for all DNA transactions, including DNA damage and repair. Chromatin organization imposes major constraints on DNA damage repair and thus undergoes critical rearrangements during the repair process. These rearrangements have been integrated into the "Access-Repair-Restore" (ARR) model, which provides a molecular framework for chromatin dynamics in response to DNA damage. Here, we take a historical perspective on the elaboration of this model and describe the molecular players involved in damaged chromatin reorganization in human cells. In particular, we present our current knowledge of chromatin assembly coupled to DNA damage repair, focusing on the role of histone variants and their dedicated chaperones. Finally, we discuss the impact of chromatin rearrangements after DNA damage on chromatin function and epigenome maintenance.

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Section: Emergence Of the Arr Model: From The Original Concepts To A mentioning

confidence: 88%

Chromatin dynamics after DNA damage: The legacy of the access–repair–restore model

2015

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“…It was thus suggested recently (Berger and Sikorski, 1981) that the stimulation of poly(ADP-ribose) synthesis during DNA excision repair may be responsible for altering the chromatin in order to facilitate the process. In fact, studies of Smerdon et al (1979), Bodel and Cleaver (1981) and Zolan et al (1982) provide evidence that excision repair processes are accompanied by extensive chromatin rearrangement in cells undergoing DNA repair synthesis caused by u.v. irradiation.…”

Section: Discussionmentioning

confidence: 99%

Correlation between endogenous nucleosomal hyper(ADP-ribosyl)ation of histone H1 and the induction of chromatin relaxation.

Aubin¹,

Fréchette²,

Murcia³

et al. 1983

The EMBO Journal

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The effect of poly(ADP‐ribose) synthesis on chromatin structure was investigated by velocity sedimentation and electron microscopy. We demonstrate that locally relaxed regions can be generated within polynucleosome chains by the activity of their intrinsic poly(ADP‐ribose)polymerase. This relaxation phenomenon is also shown to be NAD dependent and to be correlated with the formation of hyper(ADP‐ribosyl)ated forms of histone H1. Evidence is also presented which suggests that hyper(ADP‐ribosyl)ated histone H1 is neither released from the relaxed chromatin, nor does it seem to participate in polynucleosomal aggregation.

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“…We are just beginning to learn to what extent these different chromatin structures affect the distribution of damage and repair in the genome. Lesions produced by aflatoxin B1 (AFB1) (5,6), furocoumarins (7,8,9), and N-acetoxy-2-acetyl ami nofl uorene (10) are found predomi nantly in the internucleosomal linker DNA. Studies with the highly repetitive alpha DNA of African green monkey cells have shown that removal of certain bulky chemical adducts from the heterochromatic, non-transcribed alpha DNA is less efficient than is their removal from the genome overall (11)(12)(13)(14).…”

Section: Introductionmentioning

confidence: 99%

Differential repair of DNA damage in specific nucleotide sequences in monkey cells

Leadon

1986

Nucl Acids Res

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An immunological method was developed that isolates DNA fragments containing bromouracil in repair patches from unrepaired DNA using a monoclonal antibody that recognizes bromouracil. Cultured monkey cells were exposed to either UV light or the activated carcinogen aflatoxin B1 and excision repair of damage in DNA fragments containing the integrated and transcribed E. coli gpt gene was compared to that in the genome overall. A more rapid repair, of both UV and AFB1 damage was observed in the DNA fragments containing the E. coli gpt genes. The more efficient repair of UV damage was not due to a difference in the initial level of pyrimidine dimers as determined with a specific UV endonuclease. Consistent with previous observations using different methodology, repair of UV damage in the alpha sequences was found to occur at the same rate as that in the genome overall, while repair of AFB1 damage was deficient in alpha DNA. The preferential repair of damage in the gpt gene may be related to the functional state of the sequence and/or to alterations produced in the chromatin conformation by the integration of plasmid sequences carrying the gene.

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Rearrangement of mammalian chromatin structure following excision repair

Cited by 48 publications

References 21 publications

Chromatin dynamics after DNA damage: The legacy of the access–repair–restore model

Chromatin dynamics after DNA damage: The legacy of the access–repair–restore model

Correlation between endogenous nucleosomal hyper(ADP-ribosyl)ation of histone H1 and the induction of chromatin relaxation.

Differential repair of DNA damage in specific nucleotide sequences in monkey cells

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