Abstract
Histones are highly alkaline proteins that package and order the DNA into chromatin in eukaryotic cells. Nucleotide excision repair (NER) is a conserved multistep reaction that removes a wide range of generally bulky and/or helix-distorting DNA lesions. Although the core biochemical mechanism of NER is relatively well known, how cells detect and repair lesions in diverse chromatin environments is still under intensive research. As with all DNA-related processes, the NER machinery must deal with the presence of organized chromatin and the physical obstacles it presents. A huge catalogue of posttranslational histone modifications has been documented. Although a comprehensive understanding of most of these modifications is still lacking, they are believed to be important regulatory elements for many biological processes, including DNA replication and repair, transcription and cell cycle control. Some of these modifications, including acetylation, methylation, phosphorylation and ubiquitination on the four core histones (H2A, H2B, H3 and H4) or the histone H2A variant H2AX, have been found to be implicated in different stages of the NER process. This review will summarize our recent understanding in this area.
Highlights
Histones are highly alkaline proteins that package and order the DNA into chromatin in eukaryotic cells
Ordered and well-coordinated posttranslational histone modifications may be implicated in the whole process of Nucleotide excision repair (NER)
In view of the diversity and enormous possible combinations of the posttranslational histone modifications, the ones that are currently known to be implicated in NER may only represent a tip of an iceberg and the “code” of histone modifications for NER is far from being clear
Summary
Histones are highly alkaline proteins that package and order the DNA into chromatin in eukaryotic cells. A comprehensive understanding of most of these modifications is still lacking, they are believed to be important regulatory elements for many biological processes, including DNA replication and repair, transcription and cell cycle control [2]. They function by influencing chromatin contacts through structural histone changes or influencing electrostatic interactions, or by recruiting non-histone proteins to chromatin. Note that “collective” modifications, especially acetylations and ubiquitinations, at multiple sites on histones may be implicated in NER The components of these “collective” modifications have not been well-defined and are not indicated in the figure
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