Phosphorylation of H2AX at short telomeres in T cells and fibroblasts

Ling Yang Hao, Margaret A. Strong, Carol W. Greider

Research output: Contribution to journalArticlepeer-review


Eukaryotic cells undergo arrest and enter apoptosis in response to short telomeres. T cells from late generation mTR-/- mice that lack telomerase show increased apoptosis when stimulated to enter the cell cycle. The increased apoptosis was not inhibited by colcemid, indicating that the response did not result from breakage of dicentric chromosomes at mitosis. The damage response protein γ-H2AX localized to telomeres in metaphases from T cells and fibroblasts from mTR-/- cells with short telomeres. These data suggest that the major mechanism for induction of apoptosis in late generation mTR-/- cells is independent of chromosome segregation and that loss of telomere function through progressive telomere shortening in the absence of telomerase leads to recognition of telomeres as DNA breaks.

Original languageEnglish (US)
Pages (from-to)45148-45154
Number of pages7
JournalJournal of Biological Chemistry
Issue number43
StatePublished - Oct 22 2004

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Cell Biology


Dive into the research topics of 'Phosphorylation of H2AX at short telomeres in T cells and fibroblasts'. Together they form a unique fingerprint.

Cite this