Lettieri Teresa, Kraehenbuehl Rolf, Capiaghi Christoph, Livingstone-Zatchej Magdalena, Thoma Fritz
Institute of Cell Biology, ETH Zurich, Schafmattstrasse 18, CH-8093 Zurich, Switzerland.
DNA Repair (Amst). 2008 May 3;7(5):734-43. doi: 10.1016/j.dnarep.2008.01.016. Epub 2008 Mar 10.
In yeast, Rad7 and Rad16 are two proteins required for nucleotide excision repair (NER) of non-transcribed chromatin. They have roles in damage recognition, in the postincision steps of NER, and in ultraviolet-light-dependent histone H3 acetylation. Moreover, Rad16 is an ATP-ase of the SNF2 superfamily and therefore might facilitate chromatin repair by nucleosome remodelling. Here, we used yeast rad7 Delta rad16 Delta mutants and show that Rad7-Rad16 is also required for NER of UV-lesions in three functionally distinct nucleosome-free regions (NFRs), the promoter and 3'-end of the URA3 gene and the ARS1 origin of replication. Moreover, rapid repair of UV-lesions by photolyase confirmed that nucleosomes were absent and that neither UV-damage formation nor rad7 Delta rad16 Delta mutations altered chromatin accessibility in NFRs. The data are consistent with a role of Rad7-Rad16 in damage recognition and processing in absence of nucleosomes. An additional role in nucleosome remodelling is discussed.
在酵母中,Rad7和Rad16是无转录活性染色质核苷酸切除修复(NER)所需的两种蛋白质。它们在损伤识别、NER的切口后步骤以及紫外线依赖性组蛋白H3乙酰化中发挥作用。此外,Rad16是SNF2超家族的一种ATP酶,因此可能通过核小体重塑促进染色质修复。在这里,我们使用酵母rad7Δrad16Δ突变体,表明Rad7-Rad16在三个功能不同的无核小体区域(NFR),即URA3基因的启动子和3'端以及ARS1复制起点的紫外线损伤的NER中也是必需的。此外,光裂合酶对紫外线损伤的快速修复证实不存在核小体,并且紫外线损伤的形成和rad7Δrad16Δ突变均未改变NFR中的染色质可及性。这些数据与Rad7-Rad16在无核小体时的损伤识别和处理中的作用一致。文中还讨论了其在核小体重塑中的额外作用。