DERBOVEN, E., H. EKKER, B. KUSENDA, Petra BULÁNKOVÁ and Karel ŘÍHA. Role of STN1 and DNA Polymerase alpha in Telomere Stability and Genome-Wide Replication in Arabidopsis. Online. PLoS Genetics. San Francisco, California, United States: Public Library Science, 2014, vol. 10, No 10, p. "nestránkováno", 13 pp. ISSN 1553-7390. Available from: https://dx.doi.org/10.1371/journal.pgen.1004682. [citováno 2024-04-24]
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Basic information
Original name Role of STN1 and DNA Polymerase alpha in Telomere Stability and Genome-Wide Replication in Arabidopsis
Authors DERBOVEN, E. (40 Austria), H. EKKER (40 Austria), B. KUSENDA (40 Austria), Petra BULÁNKOVÁ (703 Slovakia) and Karel ŘÍHA (203 Czech Republic, guarantor, belonging to the institution)
Edition PLoS Genetics, San Francisco, California, United States, Public Library Science, 2014, 1553-7390.
Other information
Original language English
Type of outcome Article in a journal
Field of Study Genetics and molecular biology
Country of publisher United States of America
Confidentiality degree is not subject to a state or trade secret
WWW URL
Impact factor Impact factor: 7.528
RIV identification code RIV/00216224:14740/14:00079174
Organization unit Central European Institute of Technology
Doi http://dx.doi.org/10.1371/journal.pgen.1004682
UT WoS 000344650700047
Keywords in English SINGLE-STRANDED-DNA; CATALYTIC SUBUNIT; HUMAN CST; FILL-IN; CHECKPOINT ACTIVATION; DUPLEX REPLICATION; LENGTH REGULATION; CHROMOSOME ENDS; PROTEIN COMPLEX; MUTANTS
Tags kontrola MP, MP, rivok
Tags International impact, Reviewed
Changed by Changed by: Martina Prášilová, učo 342282. Changed: 23/2/2015 11:33.
Abstract
The CST (Cdc13/CTC1-STN1-TEN1) complex was proposed to have evolved kingdom specific roles in telomere capping and replication. To shed light on its evolutionary conserved function, we examined the effect of STN1 dysfunction on telomere structure in plants. STN1 inactivation in Arabidopsis leads to a progressive loss of telomeric DNA and the onset of telomeric defects depends on the initial telomere size. While EXO1 aggravates defects associated with STN1 dysfunction, it does not contribute to the formation of long G-overhangs. Instead, these G-overhangs arise, at least partially, from telomerase-mediated telomere extension indicating a deficiency in C-strand fill-in synthesis. Analysis of hypomorphic DNA polymerase a mutants revealed that the impaired function of a general replication factor mimics the telomeric defects associated with CST dysfunction. Furthermore, we show that STN1-deficiency hinders re-replication of heterochromatic regions to a similar extent as polymerase alpha mutations. This comparative analysis of stn1 and pol alpha mutants suggests that STN1 plays a genome-wide role in DNA replication and that chromosome-end deprotection in stn1 mutants may represent a manifestation of aberrant replication through telomeres.
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