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SUV39h‐ and A‐type lamin‐dependent telomere nuclear rearrangement
Author(s) -
Uhlířová Radka,
Horáková Andrea Harničarová,
Galiová Gabriela,
Legartová Soňa,
Matula Pavel,
Fojtová Miloslava,
Vařecha Miroslav,
Amrichová Jana,
Vondráček Jan,
Kozubek Stanislav,
Bártová Eva
Publication year - 2010
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.22466
Subject(s) - telomere , lamin , lmna , telomerase , trichostatin a , chromatin , histone , biology , progeria , nuclear lamina , microbiology and biotechnology , histone deacetylase , chemistry , nuclear protein , genetics , dna , nucleus , transcription factor , gene
Telomeres are specialized chromatin structures that are situated at the end of linear chromosomes and play an important role in cell senescence and immortalization. Here, we investigated whether changes in histone signature influence the nuclear arrangement and positioning of telomeres. Analysis of mouse embryonic fibroblasts revealed that telomeres were organized into specific clusters that partially associated with centromeric clusters. This nuclear arrangement was influenced by deficiency of the histone methyltransferase SUV39h, LMNA deficiency, and the histone deacetylase inhibitor Trichostatin A (TSA). Similarly, nuclear radial distributions of telomeric clusters were preferentially influenced by TSA, which caused relocation of telomeres closer to the nuclear center. Telomeres also co‐localized with promyelocytic leukemia bodies (PML). This association was increased by SUV39h deficiency and decreased by LMNA deficiency. These differences could be explained by differing levels of the telomerase subunit, TERT, in SUV39h‐ and LMNA‐deficient fibroblasts. Taken together, our data show that SUV39h and A‐type lamins likely play a key role in telomere maintenance and telomere nuclear architecture. J. Cell. Biochem. 109: 915–926, 2010. © 2010 Wiley‐Liss, Inc.