The DOI matches its Crossref record; 87 of the 87 references it cites were found in a registry or an index; none of the 49 sources its claims cite is checked for support yet.
Activation of DNA Damage Response Signaling by Condensed Chromatin
Open accessAbstract
The DNA damage response (DDR) occurs in the context of chromatin, and architectural features of chromatin have been implicated in DNA damage signaling and repair. Whereas a role of chromatin decondensation in the DDR is well established, we show here that chromatin condensation is integral to DDR signaling. We find that, in response to DNA damage chromatin regions transiently expand before undergoing extensive compaction. Using a protein-chromatin-tethering system to create defined chromatin domains, we show that interference with chromatin condensation results in failure to fully activate DDR. Conversely, forced induction of local chromatin condensation promotes ataxia telangiectasia mutated (ATM)- and ATR-dependent activation of upstream DDR signaling in a break-independent manner. Whereas persistent chromatin compaction enhanced upstream DDR signaling from irradiation-induced breaks, it reduced recovery and survival after damage. Our results demonstrate that chromatin condensation is sufficient for activation of DDR signaling and is an integral part of physiological DDR signaling.
Overview
AI snapshot
Written from the paper’s full text.
TL;DR
This paper reports that chromatin compaction is not merely a consequence of DNA damage but can itself activate upstream DNA damage response signaling. Locally condensed chromatin triggers ATM/ATR-dependent γ-H2AX and 53BP1 recruitment without detectable breaks, while persistent compaction impairs downstream signaling and survival after irradiation.
Key findings
- After localized laser damage, chromatin first expands, peaking around 1.5 min, then recompacts to baseline by 15 min and hypercondenses by 20–30 min; ASH2 overexpression dampens both the expansion and compaction phases.
- Tethering HP1α/β/γ or SUV3-9 to LacO arrays induced γ-H2AX in about 75% (HP1) or 63% (SUV3-9) of arrays and 53BP1 in about 65%, compared with 30–35% in controls, with no TUNEL, Southern blot, or LM-PCR evidence of breaks; ATM and ATR were jointly required.
- Expanded arrays caused by ASH2 tethering reduced detectable γ-H2AX and 53BP1 at I-SceI-induced breaks by about 35% despite roughly 3-fold more DSBs; condensed arrays did not activate downstream CHK2, SMC1, p53, or cell-cycle checkpoints.
- Mitotic chromosomes showed about 3-fold higher γ-H2AX than interphase without TUNEL-detectable breaks; global SUV3-9 overexpression plus 5 Gy irradiation increased NBS1 phosphorylation more than 2-fold and γ-H2AX but decreased CHK2 phosphorylation about 2-fold and markedly reduced clonogenic survival.
Methods
- Live-cell imaging in U2OS cells used photoactivatable GFP-H2A and laser microirradiation of a roughly 4.5 µm spot to track chromatin area over time; a LacO/LacR tethering system with about 10 kb arrays at two chromosomal sites created defined expanded or condensed domains, with GR-I-SceI plus dexamethasone for synchronous DSBs.
- Readouts included immunofluorescence for γ-H2AX, 53BP1, MDC1, NBS1, phospho-ATM, and H3K9me3; ChIP; nuclease accessibility; TUNEL, Southern blot, and LM-PCR for breaks; siRNA knockdown and kinase inhibitors for ATM, ATR, and DNA-PK; cell-cycle arrest; and mitotic or premature chromosome condensation analysis.
- Global damage and survival experiments used SUV3-9 overexpression plus 5 Gy γ-irradiation, Western analysis of NBS1 and CHK2 phosphorylation, and clonogenic survival assays.
Limitations
- Stated: the authors note they cannot fully exclude that co-tethering activating factors might enhance clearance of DDR factors, although they consider this unlikely.
- Evident: most evidence relies on artificial LacO tethering and overexpression in U2OS cells, so physiological relevance and behavior in other cell types are not established here.
- Evident: condensed chromatin activated only upstream DDR components, not downstream effectors or checkpoints, so the study does not show a complete DDR or repair response from condensation alone; proposed links to TIP60/ATM acetylation are discussed but not directly tested.
Model-written summary. Check it against the paper before relying on it.
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Claims the paper makes
0 of 49 cited sources checked · 0 supported · 0 flagged
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Survival of SUV3-9 expressing cells was markedly decreased compared to control cells”
§ Activation of DNA damage response signaling by condensed chromatin > Results > Condensed chromatin boosts upstream DDR signaling, but is detrimental to downstream repair and recovery
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Rests on an assumption: Overexpression of SUV3-9 globally compacts chromatin.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“phosphorylation of CHK2 decreased by about 2-fold, representing a decreased ability of DSBs in compacted chromatin environments to signal to downstream effectors”
§ Activation of DNA damage response signaling by condensed chromatin > Results > Condensed chromatin boosts upstream DDR signaling, but is detrimental to downstream repair and recovery
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Rests on an assumption: Overexpression of SUV3-9 globally compacts chromatin.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“tethering of SUV3-9 had a similar effect and led to a 2-fold increase in accumulation of γ-H2AX (63% of arrays) and recruitment of 53BP1 (65% of arrays) compared to LacR alone”
§ Activation of DNA damage response signaling by condensed chromatin > Results > Chromatin condensation triggers DDR signaling
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesA result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“γ-H2AX and 53BP1 accumulated at the I-SceI containing arrays in more than 90% of cells within 20 min”
§ Activation of DNA damage response signaling by condensed chromatin > Results > Chromatin condensation is an integral part of the DDR
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIn the paper
“tethering of SUV3-9, HP1α, −β or −γ resulted in robust accumulation of phosphorylated ATM at the array”
§ Activation of DNA damage response signaling by condensed chromatin > Results > Condensed chromatin promotes activation of upstream parts of the DDR
What the sources say
- Not checked yetcites Bakkenist and Kastan, 2003 source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIn the paper
“No labeling by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) was detected”
- Also stated in: § Chromatin condensation triggers DDR signaling · plain
“Southern blotting using probes to the Lac array did not reveal tethering-induced DSBs in the arrays”
- Also stated in: § Chromatin condensation triggers DDR signaling · plain
“no breaks were detected by ligation-mediated PCR (LM-PCR)”
§ Activation of DNA damage response signaling by condensed chromatin > Results > Chromatin condensation triggers DDR signaling
What the sources say
- Not checked yetcites Soutoglou and Misteli, 2008 source
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Rests on an assumption: The absence of detectable DNA breaks by TUNEL, Southern blot, and LM-PCR is sufficient to conclude that the DDR activation by condensed chromatin is break-independent.
- Also stated in: § Chromatin condensation triggers DDR signaling · plain
In the paper
“ASH2-expressing cells showed an ~3-fold higher level of DSBs compared to LacR expressing control cells as determined by ligation-mediated PCR”
§ Activation of DNA damage response signaling by condensed chromatin > Results > Chromatin condensation is an integral part of the DDR
What the sources say
- Not checked yetcites Soutoglou et al., 2007 source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesA result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“tethering of HP1α, −β or −γ was sufficient to trigger DDR signaling, even in the absence of DNA damage”
- Also stated in: § Chromatin condensation triggers DDR signaling · plain
“~75% of arrays showed accumulation of phospho-H2AX and ~65% showed recruitment of 53BP1 compared to 30-35% in LacR controls”
§ Activation of DNA damage response signaling by condensed chromatin > Results > Chromatin condensation triggers DDR signaling
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Also stated in: § Chromatin condensation triggers DDR signaling · plain
None of the sources cited for this claim have been checked yet.
In the paper
“an increase in γ-H2AX foci in the absence of detectable DNA breaks was observed upon premature chromosome condensation (PCC) induced by the phosphatase inhibitor Calyculin A”
§ Activation of DNA damage response signaling by condensed chromatin > Results > Condensed chromatin activates upstream components of DDR signaling in mitotic cells
What the sources say
- Not checked yetcites Coco-Martin and Begg, 1997
- Not checked yetcites Huang et al., 2006 source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesA result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“We extend these findings by demonstrating that chromatin compaction is sufficient to trigger the upstream activation of the DDR independently of the DNA lesion.”
§ Activation of DNA damage response signaling by condensed chromatin > Discussion
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes
- The quote only partly states this claim. 2
- It may state two separate claims as one. 24
- Probably not a substantial claim. 3
In the paper
“interference with chromatin condensation results in failure to fully activate DDR.”
- Also stated in: § Chromatin condensation is an integral part of the DDR · plain
“the number of arrays which showed detectable accumulation of γ-H2AX and 53BP1 was reduced by ~35% in cells with expanded chromatin arrays due to tethering of ASH2”
- Also stated in: § Discussion · plain
“interference with chromatin compaction at the site of DNA damage attenuates DDR signaling.”
§ Activation of DNA damage response signaling by condensed chromatin > Abstract
What the sources say
- Not checked yetcites Soutoglou et al., 2007 source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesThe quote only partly states this claim.
- Also stated in: § Chromatin condensation is an integral part of the DDR · plain
In the paper
“We find that upon DNA damage, chromatin regions transiently expand before undergoing extensive compaction.”
- Also stated in: § Chromatin condensation is an integral part of the DDR · plain
“This expansion was followed by an extended linear re-compaction phase, reaching pre-damage levels by 15 min, followed by hypercondensation beyond the pre-damage baseline level by 20-30 min post-damage”
- Also stated in: § Chromatin condensation is an integral part of the DDR · plain
“we conclude that the DNA damage response involves initial expansion of chromatin followed by a phase of chromatin condensation.”
§ Activation of DNA damage response signaling by condensed chromatin > Abstract
What the sources say
- Not checked yetcites Kruhlak et al., 2006 source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Also stated in: § Chromatin condensation is an integral part of the DDR · plain
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“DDR activation by chromatin condensation was not a cell cycle effect or due to stalled replication, since it was similarly observed in cells arrested either at G1/S or in G0”
§ Activation of DNA damage response signaling by condensed chromatin > Results > Chromatin condensation triggers DDR signaling
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“DDR activation was only significantly inhibited when both ATM and ATR were depleted”
- Also stated in: § Condensed chromatin promotes activation of upstream parts of the DDR · plain
“Treatment of cells containing LacR-HP1γ with specific inhibitors to both ATM and ATR, or to all three kinases led to a significant decrease in the frequency of γ-H2AX at the HP1-tethered arrays to near background levels”
- Also stated in: § Condensed chromatin promotes activation of upstream parts of the DDR · plain
“an inhibitor specific to DNA-PK did not significantly curtail phosphorylation of H2AX”
§ Activation of DNA damage response signaling by condensed chromatin > Results > Condensed chromatin promotes activation of upstream parts of the DDR
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Also stated in: § Condensed chromatin promotes activation of upstream parts of the DDR · plain
None of the sources cited for this claim have been checked yet.
In the paper
“we detect accumulation of γ-H2AX on mitotic chromosomes”
- Also stated in: § Condensed chromatin activates upstream components of DDR signaling in mitotic cells · plain
“The intensity of γ-H2AX foci on mitotic chromosomes was increased about 3-fold compared to interphase levels”
- Also stated in: § Condensed chromatin activates upstream components of DDR signaling in mitotic cells · plain
“no free DNA ends were detected on mitotic chromosomes by TUNEL”
§ Activation of DNA damage response signaling by condensed chromatin > Results > Condensed chromatin activates upstream components of DDR signaling in mitotic cells
What the sources say
- Not checked yetcites Ichijima et al., 2005 source
- Not checked yetcites McManus and Hendzel, 2005
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Also stated in: § Condensed chromatin activates upstream components of DDR signaling in mitotic cells · plain
In the paper
“tethering of ASH2 led to enrichment of the H3K4me3 mark at the array”
- Also stated in: § Chromatin condensation is an integral part of the DDR · boosted
“tethering of ASH2 led to visible expansion of array sites, demonstrating local chromatin expansion”
§ Activation of DNA damage response signaling by condensed chromatin > Results > Chromatin condensation is an integral part of the DDR
What the sources say
- Not checked yetcites Tumbar et al., 1999 source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Also stated in: § Chromatin condensation is an integral part of the DDR · boosted
None of the sources cited for this claim have been checked yet.
In the paper
“tethering of these repressive chromatin proteins led to more compact arrays”
- Also stated in: § Chromatin condensation triggers DDR signaling · plain
“tethering of HP1α, HP1γ or SUV3-9 led to enrichment of the histone H3 lysine 9 tri-methyl mark (H3K9me3) at the array”
- Also stated in: § Chromatin condensation triggers DDR signaling · plain
“tethering of heterochromatin factors also decreased accessibility to nuclease cutting”
§ Activation of DNA damage response signaling by condensed chromatin > Results > Chromatin condensation triggers DDR signaling
What the sources say
- Not checked yetcites Danzer and Wallrath, 2004
- Not checked yetcites Li et al., 2003
- Not checked yetcites Verschure et al., 2005 source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Also stated in: § Chromatin condensation triggers DDR signaling · plain
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“tethering of EZH2, a polycomb family protein involved in facultative heterochromatin formation, did not recruit DDR factors”
§ Activation of DNA damage response signaling by condensed chromatin > Results > Chromatin condensation triggers DDR signaling
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one. The quote only partly states this claim.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“these factors were not activated by tethering of HP1α, −β, or −γ”
- Also stated in: § Condensed chromatin promotes activation of upstream parts of the DDR · boosted
“Lack of activation of downstream cell cycle checkpoints by chromatin condensation was confirmed by cell-level analysis of Cyclin A immunostaining”
§ Activation of DNA damage response signaling by condensed chromatin > Results > Condensed chromatin promotes activation of upstream parts of the DDR
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Also stated in: § Condensed chromatin promotes activation of upstream parts of the DDR · boosted
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“SUV3-9 overexpressing cells showed a greater than 2-fold increase in NBS1 phosphorylation, and increased γ-H2AX, suggesting enhanced early ATM signaling”
§ Activation of DNA damage response signaling by condensed chromatin > Results > Condensed chromatin boosts upstream DDR signaling, but is detrimental to downstream repair and recovery
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Rests on an assumption: Overexpression of SUV3-9 globally compacts chromatin.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“the MDC1 mediator protein and NBS1, a component of the MRE11-RAD50-NBS1 (MRN) complex were efficiently recruited to locally compacted chromatin domains”
- Also stated in: § Condensed chromatin promotes activation of upstream parts of the DDR · plain
“typically 65-75% of arrays exhibiting recruitment, representing a 2-fold increase over control cells”
§ Activation of DNA damage response signaling by condensed chromatin > Results > Condensed chromatin promotes activation of upstream parts of the DDR
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Also stated in: § Condensed chromatin promotes activation of upstream parts of the DDR · plain
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“no DDR activation was observed upon chromatin decondensation in the absence of I-SceI cutting”
- Also stated in: § Chromatin condensation triggers DDR signaling · plain
“Tethering of chromatin expansion factors, such as ASH2, VP16, or the SWI/SNF chromatin remodeler BRG1, visibly expanded the lac arrays but, in contrast to condensed arrays, did not autonomously recruit 53BP1 or induce γ-H2AX”
§ Activation of DNA damage response signaling by condensed chromatin > Results > Chromatin condensation triggers DDR signaling
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Also stated in: § Chromatin condensation triggers DDR signaling · plain
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Both ATM and ATR contributed to the mitotic chromatin-induced DDR, as treatment with caffeine diminished pan-nuclear γ-H2AX levels further than ATM inhibition alone”
§ Activation of DNA damage response signaling by condensed chromatin > Results > Condensed chromatin activates upstream components of DDR signaling in mitotic cells
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“We take these data to suggest that HP1 does not act as a platform for DDR factor recruitment, but that condensed chromatin structures induce upstream DDR signaling.”
§ Activation of DNA damage response signaling by condensed chromatin > Results > Condensed chromatin promotes activation of upstream parts of the DDR
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“phosphorylation enhances the acetyltransferase activity of TIP60, and this modification can be induced by chromatin alterations, leading to ATM signaling independently of DNA breaks”
§ Activation of DNA damage response signaling by condensed chromatin > Introduction
What the sources say
- Not checked yetcites Kaidi and Jackson, 2013 source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim. It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“H3K9me3 is known to stimulate binding and activation of the TIP60 acetyltransferase after DNA damage”
- Also stated in: § Introduction · plain
“TIP60 in turn acetylates ATM kinase, which promotes its activation”
§ Activation of DNA damage response signaling by condensed chromatin > Introduction
What the sources say
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Also stated in: § Introduction · plain
None of the sources cited for this claim have been checked yet.
In the paper
“Local chromatin decondensation, as well as histone reorganization and eviction have been observed after experimental induction of DSBs in mammalian cells”
- Also stated in: § Introduction · plain
“expedite downstream aspects of the DDR”
§ Activation of DNA damage response signaling by condensed chromatin > Introduction
What the sources say
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Also stated in: § Introduction · plain
None of the sources cited for this claim have been checked yet.
In the paper
“HP1 tethering to lacO has been previously shown to induce chromatin compaction and silencing”
§ Activation of DNA damage response signaling by condensed chromatin > Results > Chromatin condensation triggers DDR signaling
What the sources say
- Not checked yetcites Danzer and Wallrath, 2004
- Not checked yetcites Li et al., 2003
- Not checked yetcites Verschure et al., 2005 source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“we find that condensed chromatin domains are sufficient to trigger ATM/ATR-dependent signaling and activate upstream, but not downstream, components of the DDR cascade.”
§ Activation of DNA damage response signaling by condensed chromatin > Discussion
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“while chromatin compaction enhances upstream signaling, its interference with decondensation negatively impacts repair and recovery from DNA damage.”
- Also stated in: § Discussion · plain
“While condensation can augment upstream signaling, it renders damage refractory to repair and represses the recovery of cells from DNA damage”
§ Activation of DNA damage response signaling by condensed chromatin > Results > Condensed chromatin boosts upstream DDR signaling, but is detrimental to downstream repair and recovery
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Also stated in: § Discussion · plain
None of the sources cited for this claim have been checked yet.
In the paper
“Recent work suggests that a transient repressive chromatin domain enriched in the histone H3 lysine 9 di- and tri-methyl marks is established by PRDM2 and SUV3-9 methyltransferases being recruited to DNA damage sites”
§ Activation of DNA damage response signaling by condensed chromatin > Introduction
What the sources say
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim.
In the paper
“In a recent study, SUV3-9 was shown to be recruited to DSBs, establishing the repressive H3K9me3 histone mark at sites of damage, which captures HP1, KAP-1 and further SUV3-9, propagating the heterochromatin domain for tens of kb surrounding a DSB (Ayrapetov et al., 2014).”
§ Activation of DNA damage response signaling by condensed chromatin > Discussion
What the sources say
- Not checked yetcites Ayrapetov et al., 2014 source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Taken together, these observations provide evidence that chromatin condensation is an integral, but transient step in the activation of DDR signaling, integrating observations of opposing dynamics of chromatin after damage.”
§ Activation of DNA damage response signaling by condensed chromatin > Discussion
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Formation of a H3K9me3 repressive mark creates binding sites for the TIP60 acetyltransferase, which then contributes to the amplification of ATM activity (Ayrapetov et al., 2014; Sun et al., 2005; Sun et al., 2009).”
§ Activation of DNA damage response signaling by condensed chromatin > Discussion
What the sources say
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Later, ATM signaling leads to KAP-1 phosphorylation and release of the KAP-1/HP1/SUV3-9 and CHD3 complexes, promoting the relaxation of the chromatin that is essential to downstream signaling and repair (Ayrapetov et al., 2014; Goodarzi et al., 2011; Goodarzi et al., 2008).”
§ Activation of DNA damage response signaling by condensed chromatin > Discussion
What the sources say
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“it has previously been noted that rapid activation of ATM kinase after a DSB occurs within seconds after irradiation and the majority of the relatively large cellular pool of ATM is activated by only a few strand breaks (Bakkenist and Kastan, 2003).”
§ Activation of DNA damage response signaling by condensed chromatin > Discussion
What the sources say
- Not checked yetcites Bakkenist and Kastan, 2003 source
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
The paper relies on this without support.
The absence of detectable DNA breaks by TUNEL, Southern blot, and LM-PCR is sufficient to conclude that the DDR activation by condensed chromatin is break-independent.
“Several lines of evidence rule out that DDR signaling upon array-localized chromatin condensation is the result of DNA breaks induced by tethering.”
“which sensitively amplifies DSBs near the lacO integration site”
The paper relies on this without support.
Overexpression of SUV3-9 globally compacts chromatin.
“To this end, we globally compacted chromatin by overexpressing the SUV3-9 methyltransferase”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“consistent with a role for (epi)genomic context in modulating DSB repair efficiency (44–47).”
From Controlled DNA double-strand break induction in mice reveals post-damage transcriptome stability (2016) · cites this paper as [45]
In the citing paper
“DSBs are known to promote a dynamic reorganization of break-proximal chromatin, with the potential to affect the expression of both break-proximal and ostensibly undamaged genes (10,13,19,45,48–50).”
From Controlled DNA double-strand break induction in mice reveals post-damage transcriptome stability (2016) · cites this paper as [45]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
Each contradiction between two passages listed here was confirmed by an independent check.
Reported γ-H2AX intensities reverse the stated comparison
MajorThe text says the signal was weaker in ASH2-expressing cells, but reports a higher median intensity for those cells (1043) than for controls (855). This reverses the direction of a result used to support reduced DDR signaling.
“the γ-H2AX signal at damaged arrays was slightly weaker in ASH2 expressing cells”
“ASH2 expressing cells (median intensity: 1043 +/− 308) than in control cells (855 +/− 222, p < 0.05; Fig. 1D).”
Citations
Cites
1 retracted
KAT5 tyrosine phosphorylation couples chromatin sensing to ATM signalling
Kaidi, A., & Jackson, S. P. (2013) · Nature · doi:10.1038/nature12201 · Cited by 167
RetractedThe ENCODE Project Consortium (2007) · Nature · doi:10.1038/nature05874 · Cited by 5,223
The DNA Damage Response: Making It Safe to Play with Knives
Ciccia, A., & Elledge, S. J. (2010) · Molecular Cell · doi:10.1016/j.molcel.2010.09.019 · Cited by 4,368
DNA damage activates ATM through intermolecular autophosphorylation and dimer dissociation
Bakkenist, C. J., & Kastan, M. B. (2003) · Nature · doi:10.1038/nature01368 · Cited by 3,466
Megabase Chromatin Domains Involved in DNA Double-Strand Breaks in Vivo
Rogakou, E. P., Boon, C., Redon, C., & Bonner, W. M. (1999) · The Journal of Cell Biology · doi:10.1083/jcb.146.5.905 · Cited by 2,422
Active Genes Are Tri-Methylated at K4 of Histone H3
Santos-Rosa, H., Schneider, R., Bannister, A. J., Sherriff, J., Bernstein, B. E., Emre, N. C. T., Schreiber, S. L., Mellor, J., & Kouzarides, T. (2002) · Nature · doi:10.1038/nature01080 · Cited by 2,138
ATM Phosphorylates Histone H2AX in Response to DNA Double-strand Breaks
Burma, S., Chen, B. P., Murphy, M., Kurimasa, A., & Chen, D. J. (2001) · Journal of Biological Chemistry · doi:10.1074/jbc.c100466200 · Cited by 1,954
ATM Activation by DNA Double-Strand Breaks Through the Mre11-Rad50-Nbs1 Complex
Lee, J.-H., & Paull, T. T. (2005) · Science · doi:10.1126/science.1108297 · Cited by 1,424
High-Resolution Mapping and Characterization of Open Chromatin across the Genome
Boyle, A. P., Davis, S., Shulha, H. P., Meltzer, P., Margulies, E. H., Weng, Z., Furey, T. S., & Crawford, G. E. (2008) · Cell · doi:10.1016/j.cell.2007.12.014 · Cited by 1,415
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Hirao, A., Kong, Y., Matsuoka, S., Wakeham, A. C., Ruland, J., Yoshida, H., Liu, D., Elledge, S. J., & Mak, T. W. (2000) · Science · doi:10.1126/science.287.5459.1824 · Cited by 1,311
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Li, L., Shi, L., Yang, S., Yan, R., Zhang, D., Yang, J., He, L., Li, W., Yi, X., Sun, L., et al. (2016) · Nature Communications · doi:10.1038/ncomms12235 · Cited by 400
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Hauer, M., & Gasser, S. M. (2017) · Genes & Development · doi:10.1101/gad.307702.117 · Cited by 320
Luijsterburg, M. S., de Krijger, I., Wiegant, W. W., Shah, R. G., Smeenk, G., de Groot, A. J. L., Pines, A., Vertegaal, A. C. O., Jacobs, J. J. L., Shah, G. M., et al. (2016) · Molecular Cell · doi:10.1016/j.molcel.2016.01.019 · Cited by 301
Cremer, T., Cremer, M., Hübner, B., Strickfaden, H., Smeets, D., Popken, J., Sterr, M., Markaki, Y., Rippe, K., & Cremer, C. (2015) · FEBS Letters · doi:10.1016/j.febslet.2015.05.037 · Cited by 246
Zhang, L., & Sun, C. (2018) · Applied and Environmental Microbiology · doi:10.1128/aem.00445-18 · Cited by 239
Izhar, L., Adamson, B., Ciccia, A., Lewis, J., Vaites, L. P., Leng, Y., Liang, A. C. T., Westbrook, T. F., Harper, J. W., & Elledge, S. J. (2015) · Cell Reports · doi:10.1016/j.celrep.2015.04.053 · Cited by 178
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Bao, X., Liu, Z., Zhang, W., Gladysz, K., Fung, Y. M. E., Tian, G., Xiong, Y., Wong, J. W. H., Yuen, K. W. Y., & Li, X. (2019) · Molecular Cell · doi:10.1016/j.molcel.2019.08.018 · Cited by 171
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Sharma, V., Khurana, S., Kubben, N., Abdelmohsen, K., Oberdoerffer, P., Gorospe, M., & Misteli, T. (2015) · EMBO Reports · doi:10.15252/embr.201540437 · Cited by 151
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Vítor, A. C., Huertas, P., Legube, G., & de Almeida, S. F. (2020) · Frontiers in Molecular Biosciences · doi:10.3389/fmolb.2020.00024 · Cited by 162
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Lorković, Z. J., Park, C., Goiser, M., Jiang, D., Kurzbauer, M.-T., Schlögelhofer, P., & Berger, F. (2017) · Current Biology · doi:10.1016/j.cub.2017.03.002 · Cited by 117
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Quin, J. E., Chan, K. T., Devlin, J. R., Cameron, D. P., Diesch, J., Cullinane, C. M., Ahern, J., Khot, A. S., Hein, N., George, A. J., et al. (2016) · Oncotarget · doi:10.18632/oncotarget.10452 · Cited by 110
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Li, Z., Li, Y., Tang, M., Peng, B., Lu, X., Yang, Q., Zhu, Q., Hou, T., Li, M., Liu, C., et al. (2018) · Cell Research · doi:10.1038/s41422-018-0048-0 · Cited by 100
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Osterwald, S., Deeg, K. I., Chung, I., Parisotto, D., Wörz, S., Rohr, K., Erfle, H., & Rippe, K. (2015) · Journal of Cell Science · doi:10.1242/jcs.148296 · Cited by 92
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Metadata
- Authors
- Burgess, R. C., Burman, B., Kruhlak, M. J., & Misteli, T.
- Affiliations
- National Institutes of Health (US)
- Tufts University (US)
- Corresponding author
- Misteli, Tom
- Venue
- Cell Reports
- Publisher
- Elsevier BV
- Published
- 2014-12
- Volume
- 9
- Issue
- 5
- Pages
- 1703-1717
- ISSN
- 2211-1247 (ISSN-L)
- PMC
- PMC4267891
- OpenAlex
- W2031574278
- Semantic Scholar
- 7411e97d9893b37dbc72c4708baccebd81ef2bcb
- Cited by
- 198
- References
- 87
- Citations by year
- 2026: 13 · 2025: 8 · 2024: 11 · 2023: 11 · 2022: 14 · 2021: 13 · 2020: 27 · 2019: 19 · 2018: 19 · 2017: 21 · 2016: 18 · 2015: 24
- FWCI
- 8.61
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Cell Reports (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Institutes of Health
- National Cancer Institute
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Chromatin Remodeling and Cancer
- Keywords
- DNA damage response, chromatin condensation, chromatin structure, ATM, ATR, DNA damage signaling, DNA repair
- MeSH terms
- Chromatin, DNA Damage, DNA Repair, Enzyme Activation, Humans, Protein Kinases, Signal Transduction, Chromatin Assembly and Disassembly, Cell Line, Tumor, Cell Cycle Checkpoints
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
A language model drew the claims from the paper on 2026-10-06, under version 3 of the claim definition (model deepseek-v4.1-flash, prompt extract-v3).
A second model labelled each claim on 2026-10-06 (model jev-1.13-20260917, definition revision gold-guideline-v0.2).
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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