PMID- 19079240
OWN - NLM
STAT- MEDLINE
DCOM- 20090311
LR  - 20211020
IS  - 1476-4687 (Electronic)
IS  - 0028-0836 (Linking)
VI  - 457
IP  - 7229
DP  - 2009 Jan 29
TI  - RAD6-RAD18-RAD5-pathway-dependent tolerance to chronic low-dose ultraviolet 
      light.
PG  - 612-5
LID - 10.1038/nature07580 [doi]
AB  - In nature, organisms are exposed to chronic low-dose ultraviolet light (CLUV) as 
      opposed to the acute high doses common to laboratory experiments. Analysis of the 
      cellular response to acute high-dose exposure has delineated the importance of 
      direct DNA repair by the nucleotide excision repair pathway and for 
      checkpoint-induced cell cycle arrest in promoting cell survival. Here we examine 
      the response of yeast cells to CLUV and identify a key role for the 
      RAD6-RAD18-RAD5 error-free postreplication repair (RAD6 error-free PRR) pathway 
      in promoting cell growth and survival. We show that loss of the RAD6 error-free 
      PRR pathway results in DNA-damage-checkpoint-induced G2 arrest in CLUV-exposed 
      cells, whereas wild-type and nucleotide-excision-repair-deficient cells are 
      largely unaffected. Cell cycle arrest in the absence of the RAD6 error-free PRR 
      pathway was not caused by a repair defect or by the accumulation of 
      ultraviolet-induced photoproducts. Notably, we observed increased replication 
      protein A (RPA)- and Rad52-yellow fluorescent protein foci in the CLUV-exposed 
      rad18Delta cells and demonstrated that Rad52-mediated homologous recombination is 
      required for the viability of the rad18Delta cells after release from 
      CLUV-induced G2 arrest. These and other data presented suggest that, in response 
      to environmental levels of ultraviolet exposure, the RAD6 error-free PRR pathway 
      promotes replication of damaged templates without the generation of extensive 
      single-stranded DNA regions. Thus, the error-free PRR pathway is specifically 
      important during chronic low-dose ultraviolet exposure to prevent 
      counter-productive DNA checkpoint activation and allow cells to proliferate 
      normally.
FAU - Hishida, Takashi
AU  - Hishida T
AD  - Research Institute for Microbial Diseases, Osaka University, 3-1 Yamadaoka, 
      Suita, Osaka 565-0871, Japan. hishida@biken.osaka-u.ac.jp
FAU - Kubota, Yoshino
AU  - Kubota Y
FAU - Carr, Antony M
AU  - Carr AM
FAU - Iwasaki, Hiroshi
AU  - Iwasaki H
LA  - eng
GR  - G0600233/Medical Research Council/United Kingdom
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20081214
PL  - England
TA  - Nature
JT  - Nature
JID - 0410462
RN  - 0 (DNA, Fungal)
RN  - 0 (DNA-Binding Proteins)
RN  - 0 (RAD18 protein, S cerevisiae)
RN  - 0 (RAD52 protein, S cerevisiae)
RN  - 0 (Rad52 DNA Repair and Recombination Protein)
RN  - 0 (Replication Protein A)
RN  - 0 (Saccharomyces cerevisiae Proteins)
RN  - EC 2.3.2.23 (RAD6 protein, S cerevisiae)
RN  - EC 2.3.2.23 (Ubiquitin-Conjugating Enzymes)
RN  - EC 3.6.1.- (Adenosine Triphosphatases)
RN  - EC 3.6.1.- (RAD5 protein, S cerevisiae)
RN  - EC 3.6.4.- (DNA Helicases)
SB  - IM
MH  - Adenosine Triphosphatases/deficiency/genetics/*metabolism
MH  - DNA Damage
MH  - DNA Helicases
MH  - DNA Repair/*radiation effects
MH  - DNA Replication/radiation effects
MH  - DNA, Fungal/radiation effects
MH  - DNA-Binding Proteins/deficiency/genetics/*metabolism
MH  - G2 Phase/radiation effects
MH  - Rad52 DNA Repair and Recombination Protein/metabolism
MH  - Recombination, Genetic
MH  - Replication Protein A/metabolism
MH  - Saccharomyces cerevisiae/cytology/genetics/*metabolism/*radiation effects
MH  - Saccharomyces cerevisiae Proteins/genetics/*metabolism
MH  - Ubiquitin-Conjugating Enzymes/deficiency/genetics/*metabolism
MH  - *Ultraviolet Rays
EDAT- 2008/12/17 09:00
MHDA- 2009/03/12 09:00
CRDT- 2008/12/17 09:00
PHST- 2008/03/26 00:00 [received]
PHST- 2008/10/24 00:00 [accepted]
PHST- 2008/12/17 09:00 [entrez]
PHST- 2008/12/17 09:00 [pubmed]
PHST- 2009/03/12 09:00 [medline]
AID - nature07580 [pii]
AID - 10.1038/nature07580 [doi]
PST - ppublish
SO  - Nature. 2009 Jan 29;457(7229):612-5. doi: 10.1038/nature07580. Epub 2008 Dec 14.