J 2014

Role of STN1 and DNA Polymerase alpha in Telomere Stability and Genome-Wide Replication in Arabidopsis

DERBOVEN, E., H. EKKER, B. KUSENDA, Petra BULÁNKOVÁ, Karel ŘÍHA et. al.

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

Language

English

Type of outcome

Článek v odborném periodiku

Field of Study

Genetics and molecular biology

Country of publisher

United States of America

Confidentiality degree

není předmětem státního či obchodního tajemství

References:

Impact factor

Impact factor: 7.528

RIV identification code

RIV/00216224:14740/14:00079174

Organization unit

Central European Institute of Technology

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

International impact, Reviewed
Změněno: 23/2/2015 11:33, Martina Prášilová

Abstract

V originále

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.