TY - JOUR
T1 - Nucleotide excision repair in chromatin and the right of entry
AU - Gong, Feng
AU - Kwon, Youngho
AU - Smerdon, Michael J.
N1 - Funding Information:
This work was made possible by NIH grants ES04106 and ES02614 from the National Institute of Environmental Health Sciences (NIEHS). Its contents are solely the responsibility of the authors and do not necessarily represent the official views of the NIEHS, NIH.
PY - 2005/7/28
Y1 - 2005/7/28
N2 - DNA is packaged with histones and other accessory proteins into chromatin in eukaryotic cells. It is well established that the assembly of DNA into chromatin affects induction of DNA damage as well as repair of the damage. How the DNA repair machinery detects a lesion and 'fixes it' in chromatin has been an intriguing question since the dawn of understanding DNA packaging in chromatin. Direct recognition/binding by damaged DNA binding proteins is one obvious tactic to detect a lesion. Rearrangement of chromatin structure during DNA repair was reported more than two decades ago. This early observation suggests that unfolding of chromatin structure may be required to facilitate DNA repair after lesions are detected. Cells can also exploit DNA processing events to assist DNA repair. Transcription coupled repair (TCR) is such an example. During TCR, an RNA polymerase blocked by a lesion, may act as a signal to recruit DNA repair machinery. Possible roles of histone modification enzymes, ATP-dependent chromatin remodeling complexes and chromatin assembly factors in DNA repair are discussed.
AB - DNA is packaged with histones and other accessory proteins into chromatin in eukaryotic cells. It is well established that the assembly of DNA into chromatin affects induction of DNA damage as well as repair of the damage. How the DNA repair machinery detects a lesion and 'fixes it' in chromatin has been an intriguing question since the dawn of understanding DNA packaging in chromatin. Direct recognition/binding by damaged DNA binding proteins is one obvious tactic to detect a lesion. Rearrangement of chromatin structure during DNA repair was reported more than two decades ago. This early observation suggests that unfolding of chromatin structure may be required to facilitate DNA repair after lesions are detected. Cells can also exploit DNA processing events to assist DNA repair. Transcription coupled repair (TCR) is such an example. During TCR, an RNA polymerase blocked by a lesion, may act as a signal to recruit DNA repair machinery. Possible roles of histone modification enzymes, ATP-dependent chromatin remodeling complexes and chromatin assembly factors in DNA repair are discussed.
KW - Cyclobutane pyrimidine dimer
KW - Designed nucleosomes
KW - Histones
KW - Transcription coupled repair
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U2 - 10.1016/j.dnarep.2005.04.007
DO - 10.1016/j.dnarep.2005.04.007
M3 - Review article
C2 - 15961354
AN - SCOPUS:21844434955
VL - 4
SP - 884
EP - 896
JO - DNA Repair
JF - DNA Repair
SN - 1568-7864
IS - 8
ER -