10.5061/DRYAD.H1157
Vancevska, Aleksandra
École Polytechnique Fédérale de Lausanne
Douglass, Kyle M.
École Polytechnique Fédérale de Lausanne
Pfeiffer, Verena
École Polytechnique Fédérale de Lausanne
Manley, Suliana
École Polytechnique Fédérale de Lausanne
Lingner, Joachim
École Polytechnique Fédérale de Lausanne
Data from: The telomeric DNA damage response occurs in the absence of
chromatin decompaction
Dryad
dataset
2018
STORM
2018-04-04T00:00:00Z
2018-04-04T00:00:00Z
en
https://doi.org/10.1101/gad.294082.116
23195123391 bytes
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CC0 1.0 Universal (CC0 1.0) Public Domain Dedication
Telomeres are specialized nucleoprotein structures that protect chromosome
ends from DNA damage response (DDR) and DNA rearrangements. The telomeric
shelterin protein TRF2 suppresses the DDR, and this function has been
attributed to its abilities to trigger t-loop formation or prevent massive
decompaction and loss of density of telomeric chromatin. Here, we applied
stochastic optical reconstruction microscopy (STORM) to measure the sizes
and shapes of functional human telomeres of different lengths and
dysfunctional telomeres that elicit a DDR. Telomeres have an ovoid
appearance with considerable plasticity in shape. Examination of many
telomeres demonstrated that depletion of TRF2, TRF1, or both affected the
sizes of only a small subset of telomeres. Costaining of telomeres with
DDR markers further revealed that the majority of DDR signaling telomeres
retained a normal size. Thus, DDR signaling at telomeres does not require
decompaction. We propose that telomeres are monitored by the DDR machinery
in the absence of telomere expansion and that the DDR is triggered by
changes at the molecular level in structure and protein composition.
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