Detection of bulky DNA lesions: DDB2 at the interface of chromatin and DNA repair in eukaryotes

Jones, Kristi L.; Zhang, Ling; Seldeen, Kenneth L.; Gong, Feng

doi:10.1002/iub.391

Cited by 10 publications

(10 citation statements)

References 98 publications

(115 reference statements)

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“…This observation has led to the idea that DDB-mediated photolesion recognition may link chromatin remodeling to DNA repair [49]. To support this notion, INO80 chromatin remodeling complex was shown to promote the removal of UV lesions.…”

Section: Discussionmentioning

confidence: 99%

Damaged DNA-binding protein down-regulates epigenetic mark H3K56Ac through histone deacetylase 1 and 2

Zhu

Battu

Ray

et al. 2015

Mutation Research/Fundamental and Molecular Mechanisms of Mutag

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Acetylated histone H3 lysine 56 (H3K56Ac) is one of the reversible histone post-translational modifications (PTMs) responsive to DNA damage. We previously described a biphasic decrease and increase of epigenetic mark H3K56Ac in response to ultraviolet radiation (UVR)-induced DNA damage. Here, we report a new function of UV damaged DNA-binding protein (DDB) in deacetylation of H3K56Ac through specific histone deacetylases (HDACs). We show that simultaneous depletion of HDAC1/2 compromises the deacetylation of H3K56Ac, while depletion of HDAC1 or HDAC2 alone has no effect on H3K56Ac. The H3K56Ac deacetylation does not require functional nucleotide excision repair (NER) factors XPA and XPC, but depends on the function of upstream factors DDB1 and DDB2. UVR enhances the association of DDB2 with HDAC1 and, enforced DDB2 expression leads to translocation of HDAC1 to UVR-damaged chromatin. HDAC1 and HDAC2 are recruited to UVR-induced DNA damage spots, which are visualized by anti-XPC immunofluorescence. Dual HDAC1/2 depletion decreases XPC ubiquitination, but does not affect the recruitment of DDB2 to DNA damage. By contrast, the local accumulation of γH2AX at UVR-induced DNA damage spots was compromised upon HDAC1 as well as dual HDAC1/2 depletions. Additionally, UVR-induced ATM activation decreased in H12899 cells expressing H3K56Ac-mimicing H3K56Q. These results revealed a novel role of DDB in H3K56Ac deacetylation during early step of NER and the existence of active functional cross-talk between DDB-mediated damage recognition and H3K56Ac deacetylation.

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Section: Discussionmentioning

confidence: 99%

Damaged DNA-binding protein down-regulates epigenetic mark H3K56Ac through histone deacetylase 1 and 2

Zhu

Battu

Ray

et al. 2015

Mutation Research/Fundamental and Molecular Mechanisms of Mutag

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“…Although several chromatin remodeling activities have been linked to NER (Jiang et al, 2010; Lans et al, 2010), the underlying mechanisms are poorly understood. The observation that the lesion recognition protein DDB2 is nonessential for NER in vitro but is required for CPD repair and significantly promotes 6-4PP repair in vivo (Hwang et al, 1999; Tang et al, 2000; Moser et al, 2005) has led to the idea that this early NER factor may link chromatin remodeling to DNA repair (Jones et al, 2010; Palomera-Sanchez and Zurita, 2011).…”

Section: Discussionmentioning

confidence: 99%

DDB2 promotes chromatin decondensation at UV-induced DNA damage

Luijsterburg

Lindh

Ács

et al. 2012

Journal of Cell Biology

134

147

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“…However, it remains unclear whether the tumor suppressor functions of ACRs require ACR-mediated chromatin remodeling [13]. Several recent reviews discuss various aspects of chromatin remodeling and NER [15–20]. This review will specifically focus on the role of ACRs enzymes in regulation of NER in chromatin.…”

Section: Chromatin Structure and Dna Accessibilitymentioning

confidence: 99%

The Emerging Roles of ATP-Dependent Chromatin Remodeling Enzymes in Nucleotide Excision Repair

Czaja

Mao

Smerdon

2012

IJMS

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DNA repair in eukaryotic cells takes place in the context of chromatin, where DNA, including damaged DNA, is tightly packed into nucleosomes and higher order chromatin structures. Chromatin intrinsically restricts accessibility of DNA repair proteins to the damaged DNA and impacts upon the overall rate of DNA repair. Chromatin is highly responsive to DNA damage and undergoes specific remodeling to facilitate DNA repair. How damaged DNA is accessed, repaired and restored to the original chromatin state, and how chromatin remodeling coordinates these processes in vivo, remains largely unknown. ATP-dependent chromatin remodelers (ACRs) are the master regulators of chromatin structure and dynamics. Conserved from yeast to humans, ACRs utilize the energy of ATP to reorganize packing of chromatin and control DNA accessibility by sliding, ejecting or restructuring nucleosomes. Several studies have demonstrated that ATP-dependent remodeling activity of ACRs plays important roles in coordination of spatio-temporal steps of different DNA repair pathways in chromatin. This review focuses on the role of ACRs in regulation of various aspects of nucleotide excision repair (NER) in the context of chromatin. We discuss current understanding of ATP-dependent chromatin remodeling by various subfamilies of remodelers and regulation of the NER pathway in vivo.

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Detection of bulky DNA lesions: DDB2 at the interface of chromatin and DNA repair in eukaryotes

Cited by 10 publications

References 98 publications

Damaged DNA-binding protein down-regulates epigenetic mark H3K56Ac through histone deacetylase 1 and 2

Damaged DNA-binding protein down-regulates epigenetic mark H3K56Ac through histone deacetylase 1 and 2

DDB2 promotes chromatin decondensation at UV-induced DNA damage

The Emerging Roles of ATP-Dependent Chromatin Remodeling Enzymes in Nucleotide Excision Repair

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