Defective Artemis causes mild telomere dysfunction.

ABSTRACT:

Background

Repair of DNA double strand breaks by non-homologous end joining (NHEJ) requires several proteins including Ku, DNA-PKcs, Artemis, XRCC4, Ligase IV and XLF. Two of these proteins, namely Ku and DNA-PKcs, are also involved in maintenance of telomeres, chromosome end-structures. In contrast, cells defective in Ligase IV and XRCC4 do not show changes in telomere length or function suggesting that these proteins are not involved in telomere maintenance. Since a mouse study indicated that defective Artemis may cause telomere dysfunction we investigated the effects of defective Artemis on telomere maintenance in human cells.

Results

We observed significantly elevated frequencies of telomeric fusions in two primary fibroblast cell lines established from Artemis defective

SUBMITTER: Yasaei H 

PROVIDER: S-EPMC2907561 | biostudies-literature | 2010 May

REPOSITORIES: biostudies-literature