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The emerging roles of ATP-dependent chromatin remodeling enzymes in nucleotide excision repair.

Czaja W, Mao P, Smerdon MJ - Int J Mol Sci (2012)

Bottom Line: 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.We discuss current understanding of ATP-dependent chromatin remodeling by various subfamilies of remodelers and regulation of the NER pathway in vivo.

View Article: PubMed Central - PubMed

Affiliation: Biochemistry and Biophysics, School of Molecular Biosciences, Washington State University, Pullman, WA, USA; E-Mails: wiolettapyrzak@vetmed.wsu.edu (W.C.); pengmao@vetmed.wsu.edu (P.M.).

ABSTRACT
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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Model demonstrating involvement of ATP-dependent chromatin remodelers (ACRs) in Global Genome Nucleotide Excision Repair (GG-NER). UV DNA lesions (red triangle) induce variety of histone modifications such as acetylation, methylation, ubiquitination. These modifications serve as signals for recruitment of ACRs and damage binding NER proteins to the damage site. The early Nucleotide Excision Repair (NER) proteins (Rad7/Rad16 and Rad4-23, DDB2/DDB1 and XPC, HR23B) arrive at the damage site, recognize and specifically bind UV lesions. Chromatin remodelers, SWI/SNF and INO80 are recruited by histone modifications and/or interactions with damage binding proteins (red double head arrows). Yeast and human ACRs are distinguished by color coding. Yeast SWI/SNF (light green), human SWI/SNF (orange), yeast INO80 (dark blue), human INO80 (purple). Remodelers catalyze chromatin remodeling (nucleosome sliding, ejection), facilitate accessibility of damaged DNA and help recruitment and assembly of the downstream NER repair proteins. The UV lesions are efficiently removed. Chromatin structure is restored to the original state potentially by nucleosome rearrangements such as octamer sliding or deposition which involves action of ACR.
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f2-ijms-13-11954: Model demonstrating involvement of ATP-dependent chromatin remodelers (ACRs) in Global Genome Nucleotide Excision Repair (GG-NER). UV DNA lesions (red triangle) induce variety of histone modifications such as acetylation, methylation, ubiquitination. These modifications serve as signals for recruitment of ACRs and damage binding NER proteins to the damage site. The early Nucleotide Excision Repair (NER) proteins (Rad7/Rad16 and Rad4-23, DDB2/DDB1 and XPC, HR23B) arrive at the damage site, recognize and specifically bind UV lesions. Chromatin remodelers, SWI/SNF and INO80 are recruited by histone modifications and/or interactions with damage binding proteins (red double head arrows). Yeast and human ACRs are distinguished by color coding. Yeast SWI/SNF (light green), human SWI/SNF (orange), yeast INO80 (dark blue), human INO80 (purple). Remodelers catalyze chromatin remodeling (nucleosome sliding, ejection), facilitate accessibility of damaged DNA and help recruitment and assembly of the downstream NER repair proteins. The UV lesions are efficiently removed. Chromatin structure is restored to the original state potentially by nucleosome rearrangements such as octamer sliding or deposition which involves action of ACR.

Mentions: Evolutionarily conserved ATP-dependent chromatin remodeling complexes have emerged as master regulators of DNA repair pathways in chromatin. ACRs facilitate GG-NER in chromatin in both yeast and human systems. ACRs remodel damaged chromatin, facilitate accessibility of damaged DNA, help recruitment and sequential assembly of NER proteins and contribute to restoration of chromatin structure. Recent studies have provided significant results directly linking ACRs with chromatin remodeling during NER (Figure 2, Table 1). Further studies are necessary to delineate more of the mechanistic details that integrate changes in chromatin structure and dynamics with efficient DNA repair.


The emerging roles of ATP-dependent chromatin remodeling enzymes in nucleotide excision repair.

Czaja W, Mao P, Smerdon MJ - Int J Mol Sci (2012)

Model demonstrating involvement of ATP-dependent chromatin remodelers (ACRs) in Global Genome Nucleotide Excision Repair (GG-NER). UV DNA lesions (red triangle) induce variety of histone modifications such as acetylation, methylation, ubiquitination. These modifications serve as signals for recruitment of ACRs and damage binding NER proteins to the damage site. The early Nucleotide Excision Repair (NER) proteins (Rad7/Rad16 and Rad4-23, DDB2/DDB1 and XPC, HR23B) arrive at the damage site, recognize and specifically bind UV lesions. Chromatin remodelers, SWI/SNF and INO80 are recruited by histone modifications and/or interactions with damage binding proteins (red double head arrows). Yeast and human ACRs are distinguished by color coding. Yeast SWI/SNF (light green), human SWI/SNF (orange), yeast INO80 (dark blue), human INO80 (purple). Remodelers catalyze chromatin remodeling (nucleosome sliding, ejection), facilitate accessibility of damaged DNA and help recruitment and assembly of the downstream NER repair proteins. The UV lesions are efficiently removed. Chromatin structure is restored to the original state potentially by nucleosome rearrangements such as octamer sliding or deposition which involves action of ACR.
© Copyright Policy - open-access
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC3472786&req=5

f2-ijms-13-11954: Model demonstrating involvement of ATP-dependent chromatin remodelers (ACRs) in Global Genome Nucleotide Excision Repair (GG-NER). UV DNA lesions (red triangle) induce variety of histone modifications such as acetylation, methylation, ubiquitination. These modifications serve as signals for recruitment of ACRs and damage binding NER proteins to the damage site. The early Nucleotide Excision Repair (NER) proteins (Rad7/Rad16 and Rad4-23, DDB2/DDB1 and XPC, HR23B) arrive at the damage site, recognize and specifically bind UV lesions. Chromatin remodelers, SWI/SNF and INO80 are recruited by histone modifications and/or interactions with damage binding proteins (red double head arrows). Yeast and human ACRs are distinguished by color coding. Yeast SWI/SNF (light green), human SWI/SNF (orange), yeast INO80 (dark blue), human INO80 (purple). Remodelers catalyze chromatin remodeling (nucleosome sliding, ejection), facilitate accessibility of damaged DNA and help recruitment and assembly of the downstream NER repair proteins. The UV lesions are efficiently removed. Chromatin structure is restored to the original state potentially by nucleosome rearrangements such as octamer sliding or deposition which involves action of ACR.
Mentions: Evolutionarily conserved ATP-dependent chromatin remodeling complexes have emerged as master regulators of DNA repair pathways in chromatin. ACRs facilitate GG-NER in chromatin in both yeast and human systems. ACRs remodel damaged chromatin, facilitate accessibility of damaged DNA, help recruitment and sequential assembly of NER proteins and contribute to restoration of chromatin structure. Recent studies have provided significant results directly linking ACRs with chromatin remodeling during NER (Figure 2, Table 1). Further studies are necessary to delineate more of the mechanistic details that integrate changes in chromatin structure and dynamics with efficient DNA repair.

Bottom Line: 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.We discuss current understanding of ATP-dependent chromatin remodeling by various subfamilies of remodelers and regulation of the NER pathway in vivo.

View Article: PubMed Central - PubMed

Affiliation: Biochemistry and Biophysics, School of Molecular Biosciences, Washington State University, Pullman, WA, USA; E-Mails: wiolettapyrzak@vetmed.wsu.edu (W.C.); pengmao@vetmed.wsu.edu (P.M.).

ABSTRACT
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.

Show MeSH
Related in: MedlinePlus