Heat shock-induced dissociation of TRF2 from telomeres does not initiate a telomere-dependent DNA damage response

Nadezhda V Petrova; Artem K Velichko; Omar L Kantidze; Sergey V Razin

doi:10.1002/cbin.10252

Heat shock-induced dissociation of TRF2 from telomeres does not initiate a telomere-dependent DNA damage response

Cell Biol Int. 2014 May;38(5):675-81. doi: 10.1002/cbin.10252. Epub 2014 Feb 6.

Authors

Nadezhda V Petrova¹, Artem K Velichko, Omar L Kantidze, Sergey V Razin

Affiliation

¹ Laboratory of Structural and Functional Organization of Chomosomes, Institute of Gene Biology, Russian Academy of Sciences, Moscow, Russia; Department of Molecular Biology, Lomonosov Moscow State University, Moscow, Russia.

PMID: 24474557
DOI: 10.1002/cbin.10252

Abstract

Telomeric repeat binding factor 2 (TRF2) is a well-studied shelterin complex subunit that plays a major role in the protection of chomosome ends and the prevention of the telomere-associated DNA damage response. We show that heat shock induces the dissociation of TRF2 from telomeres in human primary and cancer cell cultures. TRF2 is not simply degraded in response to heat shock, but redistributed thoughout the nucleoplasm. This TRF2 depletion/redistribution does not initiate the DNA damage response at chomosome termini.

Keywords: 53BP1; DNA damage response; TRF2; heat shock; heat shock response; telomeres; γH2AX.

Publication types

Research Support, Non-U.S. Gov't

MeSH terms

Cell Line
DNA Damage / physiology*
Fibroblasts / metabolism
Hot Temperature / adverse effects*
Humans
MCF-7 Cells
Telomere / genetics
Telomere / metabolism*
Telomeric Repeat Binding Protein 2 / metabolism*

Substances

TERF2 protein, human
Telomeric Repeat Binding Protein 2