PMID- 23390378
OWN - NLM
STAT- MEDLINE
DCOM- 20130530
LR  - 20211021
IS  - 1553-7404 (Electronic)
IS  - 1553-7390 (Print)
IS  - 1553-7390 (Linking)
VI  - 9
IP  - 1
DP  - 2013
TI  - Telomerase-null survivor screening identifies novel telomere recombination 
      regulators.
PG  - e1003208
LID - 10.1371/journal.pgen.1003208 [doi]
LID - e1003208
AB  - Telomeres are protein-DNA structures found at the ends of linear chromosomes and 
      are crucial for genome integrity. Telomeric DNA length is primarily maintained by 
      the enzyme telomerase. Cells lacking telomerase will undergo senescence when 
      telomeres become critically short. In Saccharomyces cerevisiae, a very small 
      percentage of cells lacking telomerase can remain viable by lengthening telomeres 
      via two distinct homologous recombination pathways. These "survivor" cells are 
      classified as either Type I or Type II, with each class of survivor possessing 
      distinct telomeric DNA structures and genetic requirements. To elucidate the 
      regulatory pathways contributing to survivor generation, we knocked out the 
      telomerase RNA gene TLC1 in 280 telomere-length-maintenance (TLM) gene mutants 
      and examined telomere structures in post-senescent survivors. We uncovered new 
      functional roles for 10 genes that affect the emerging ratio of Type I versus 
      Type II survivors and 22 genes that are required for Type II survivor generation. 
      We further verified that Pif1 helicase was required for Type I recombination and 
      that the INO80 chromatin remodeling complex greatly affected the emerging 
      frequency of Type I survivors. Finally, we found the Rad6-mediated ubiquitination 
      pathway and the KEOPS complex were required for Type II recombination. Our data 
      provide an independent line of evidence supporting the idea that these genes play 
      important roles in telomere dynamics.
FAU - Hu, Yan
AU  - Hu Y
AD  - The State Key Laboratory of Molecular Biology, Shanghai Institute of Biochemistry 
      and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of 
      Sciences, University of Chinese Academy of Sciences, Shanghai, China.
FAU - Tang, Hong-Bo
AU  - Tang HB
FAU - Liu, Ning-Ning
AU  - Liu NN
FAU - Tong, Xia-Jing
AU  - Tong XJ
FAU - Dang, Wei
AU  - Dang W
FAU - Duan, Yi-Min
AU  - Duan YM
FAU - Fu, Xiao-Hong
AU  - Fu XH
FAU - Zhang, Yang
AU  - Zhang Y
FAU - Peng, Jing
AU  - Peng J
FAU - Meng, Fei-Long
AU  - Meng FL
FAU - Zhou, Jin-Qiu
AU  - Zhou JQ
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20130117
PL  - United States
TA  - PLoS Genet
JT  - PLoS genetics
JID - 101239074
RN  - 0 (Fungal Proteins)
RN  - 0 (Saccharomyces cerevisiae Proteins)
RN  - 0 (telomerase RNA)
RN  - 63231-63-0 (RNA)
RN  - EC 2.7.7.49 (Telomerase)
RN  - EC 3.6.1.- (PIF1 protein, S cerevisiae)
RN  - EC 3.6.4.- (DNA Helicases)
SB  - IM
MH  - Chromosomes/genetics
MH  - *DNA Helicases/genetics/metabolism
MH  - Fungal Proteins/genetics/metabolism
MH  - Genomic Instability
MH  - *Homologous Recombination
MH  - RNA/genetics/metabolism
MH  - *Saccharomyces cerevisiae/genetics/metabolism
MH  - *Saccharomyces cerevisiae Proteins/genetics/metabolism
MH  - Signal Transduction
MH  - Telomerase/*genetics/metabolism
MH  - Telomere/genetics
MH  - Telomere Homeostasis/genetics
MH  - Ubiquitination
PMC - PMC3547846
COIS- The authors have declared that no competing interests exist.
EDAT- 2013/02/08 06:00
MHDA- 2013/06/01 06:00
PMCR- 2013/01/01
CRDT- 2013/02/08 06:00
PHST- 2012/02/17 00:00 [received]
PHST- 2012/11/12 00:00 [accepted]
PHST- 2013/02/08 06:00 [entrez]
PHST- 2013/02/08 06:00 [pubmed]
PHST- 2013/06/01 06:00 [medline]
PHST- 2013/01/01 00:00 [pmc-release]
AID - PGENETICS-D-12-00408 [pii]
AID - 10.1371/journal.pgen.1003208 [doi]
PST - ppublish
SO  - PLoS Genet. 2013;9(1):e1003208. doi: 10.1371/journal.pgen.1003208. Epub 2013 Jan 
      17.