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.
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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.
Integrity signals
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Cites
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Claims the paper makes
0 of 49 cited sources checked · 0 supported · 0 flagged
- Findingown data
SUV3-9 overexpression reduces clonogenic survival after DNA damage.
“Survival of SUV3-9 expressing cells was markedly decreased compared to control cells”
Quote in the paperSubstantial claim- Rests on an assumption: Overexpression of SUV3-9 globally compacts chromatin.
- Findingown data
Global chromatin compaction by SUV3-9 overexpression decreases downstream CHK2 phosphorylation by about 2-fold after γ-irradiation.
“phosphorylation of CHK2 decreased by about 2-fold, representing a decreased ability of DSBs in compacted chromatin environments to signal to downstream effectors”
Quote in the paperSubstantial claim- Rests on an assumption: Overexpression of SUV3-9 globally compacts chromatin.
- Findingown data
Tethering SUV3-9 to lacO arrays similarly triggers DDR signaling, with about 2-fold increase in γ-H2AX and 53BP1 accumulation compared to LacR controls.
“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”
Quote in the paperSubstantial claim - Findingown data
In control cells, γ-H2AX and 53BP1 accumulate at I-SceI arrays in >90% of cells within 20 min.
“γ-H2AX and 53BP1 accumulated at the I-SceI containing arrays in more than 90% of cells within 20 min”
Quote in the paperSubstantial claim - Findingown data
Tethering SUV3-9, HP1α, HP1β, or HP1γ results in robust accumulation of phosphorylated ATM at the array.
“tethering of SUV3-9, HP1α, −β or −γ resulted in robust accumulation of phosphorylated ATM at the array”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Bakkenist and Kastan, 2003 source
Not checked in the free run.
- Findingown data
The DDR activation by condensed chromatin is not due to DNA breaks induced by tethering, as no breaks were detected by TUNEL, Southern blot, or LM-PCR.
“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)”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Soutoglou and Misteli, 2008 source
Not checked in the free run.
- 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
- Findingown data
ASH2-expressing cells have ~3-fold higher DSBs than control cells after 20 min of break induction.
“ASH2-expressing cells showed an ~3-fold higher level of DSBs compared to LacR expressing control cells as determined by ligation-mediated PCR”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Soutoglou et al., 2007 source
Not checked in the free run.
- Findingown data
Tethering HP1α, HP1β, or HP1γ to lacO arrays is sufficient to trigger DDR signaling (γ-H2AX and 53BP1 accumulation) in the absence of DNA damage.
“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”
Quote in the paperSubstantial claim - Also stated in: § Chromatin condensation triggers DDR signaling · plain
- Findingcitation
Premature chromosome condensation induced by Calyculin A increases γ-H2AX foci without detectable DNA breaks.
“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”
Quote in the paperSubstantial claim0 of 2 sources checked- cites Coco-Martin and Begg, 1997
Not checked in the free run.
- cites Huang et al., 2006 source
Not checked in the free run.
- Findingown data
Compacted chromatin is enough to activate upstream DDR signaling even when no DNA lesion is present.
“We extend these findings by demonstrating that chromatin compaction is sufficient to trigger the upstream activation of the DDR independently of the DNA lesion.”
Quote in the paperSubstantial claim - Findingown data
Decompacting chromatin by overexpressing or tethering the ASH2 H3K4 methyltransferase reduces the DDR and local chromatin dynamics after damage.
“In agreement, we find that the establishment of a H3K9 methyl domain can promote signaling, while decompaction of chromatin by overexpression or tethering of the ASH2 H3K4 methyltransferase dampens the DDR and local dynamics of chromatin after damage.”
Quote in the paperSubstantial claim - Findingown data
Establishing a H3K9 methyl domain can promote DDR signaling.
“In agreement, we find that the establishment of a H3K9 methyl domain can promote signaling, while decompaction of chromatin by overexpression or tethering of the ASH2 H3K4 methyltransferase dampens the DDR and local dynamics of chromatin after damage.”
Quote in the paperSubstantial claim - Interpretationreasoning
Efficient DDR in physiological settings requires coordinated chromatin decondensation and condensation events.
“these findings highlight the need for coordinated chromatin decondensation as well as condensation events for efficient activation of the DDR in a physiological setting.”
Quote in the paperSubstantial claim - Interpretationown data
The reductions in γ-H2AX and 53BP1 in ASH2-expressing cells are not due to lower DSB induction.
“the reductions in γ-H2AX and 53BP1 were not due to lower levels of DSB induction in ASH2-expressing cells.”
Quote in the paperSubstantial claim - Premisecitation
A DNA lesion is not required for the DNA damage response machinery.
“This conclusion is in line with earlier tethering experiments demonstrating that a DNA lesion is not an obligatory part of the DDR machinery and DDR signaling can occur in its absence, allowing for the possibility of DDR initiation by stimuli other than DNA damage, such as chromatin structure (Bonilla et al., 2008; Soutoglou and Misteli, 2008).”
Quote in the paperSubstantial claim0 of 2 sources checked - Interpretationown data
Chromatin condensation is an integral step in the damage response.
“we propose that condensation of chromatin is an integral step in the damage response.”
Quote in the paperSubstantial claim - Interpretationown data
Changes in chromatin structure actively contribute to DDR activation, not just as bystanders.
“These observations suggest that changes in chromatin structure are not just bystanders, but actively contribute to DDR activation.”
Quote in the paperSubstantial claim - Interpretationcitation
The general DNA damage response includes chromatin compaction as a core component.
“This study and recently published work shows that chromatin compaction is an integral part of the generic DNA damage response (Ayrapetov et al., 2014; Khurana et al., 2014).”
Quote in the paperSubstantial claim0 of 2 sources checked - Interpretationown data
Upstream parts of the DDR are activated in naturally occurring highly condensed mitotic chromosomes.
“Fitting with a role of highly condensed chromatin as a trigger for DDR signaling, we find upstream parts of the DDR activated in naturally occurring highly condensed mitotic chromosomes.”
Quote in the paperSubstantial claim - Premisecitation
Proteins that promote chromatin compaction are recruited to DSB sites.
“proteins that promote chromatin compaction, such as HP1, KAP-1, SPOC1, su(var)3-9 methyltransferase variant 1 (SUV3-9), PDRM2 methyltransferase, macro H2A, and histone deacetylases (HDACs), have also been shown to be recruited to the sites of DSBs”
Quote in the paperSubstantial claim0 of 3 sources checked - Interpretationown data
Condensed chromatin is sufficient to stimulate DDR signaling.
“Taken together, these data suggest that condensed chromatin is sufficient to stimulate DDR signaling.”
Quote in the paperSubstantial claim - Premisecitation
DNA damage response signaling can happen without a DNA lesion.
“This conclusion is in line with earlier tethering experiments demonstrating that a DNA lesion is not an obligatory part of the DDR machinery and DDR signaling can occur in its absence, allowing for the possibility of DDR initiation by stimuli other than DNA damage, such as chromatin structure (Bonilla et al., 2008; Soutoglou and Misteli, 2008).”
Quote in the paperSubstantial claim0 of 2 sources checked - Interpretationcitation
A compact chromatin domain that enhances DDR signaling complements the need for chromatin relaxation to amplify and activate DDR effector pathways.
“The establishment of a compact chromatin domain for enhancing DDR signaling is complementary to the observation that chromatin relaxation is required for amplification and activation of DDR effector pathways, and they likely occur in a dynamic exchange (Burgess et al., 2012; Soria et al., 2012).”
Quote in the paperSubstantial claim0 of 2 sources checked - Premisecitation
Depleting SUV3-9, PRDM2 or HP1 reduces survival after DNA damage.
“Establishing the repressive chromatin domain is also important for the outcome of the DDR, as SUV3-9, PRDM2 or HP1-depletion impairs survival after DNA damage, and may shift repair pathway choice (Ayrapetov et al., 2014; Baldeyron et al., 2011; Khurana et al., 2014; Soria and Almouzni, 2013).”
Quote in the paperSubstantial claim0 of 3 sources checked - Interpretationcitation
Chromatin compaction and relaxation probably occur in a dynamic exchange.
“The establishment of a compact chromatin domain for enhancing DDR signaling is complementary to the observation that chromatin relaxation is required for amplification and activation of DDR effector pathways, and they likely occur in a dynamic exchange (Burgess et al., 2012; Soria et al., 2012).”
Quote in the paperSubstantial claim0 of 2 sources checked - Interpretationcitation
Establishing the repressive chromatin domain is important for the outcome of the DNA damage response.
“Establishing the repressive chromatin domain is also important for the outcome of the DDR, as SUV3-9, PRDM2 or HP1-depletion impairs survival after DNA damage, and may shift repair pathway choice (Ayrapetov et al., 2014; Baldeyron et al., 2011; Khurana et al., 2014; Soria and Almouzni, 2013).”
Quote in the paperSubstantial claim - Interpretationcitation
The speed and extent of DNA damage response activation imply that cells have mechanisms that detect the damage signal very efficiently.
“This rapid and extensive activation of the DDR suggests the existence of cellular mechanisms that sense the damage signal with exquisite efficiency.”
Quote in the paperNot a substantial claim - Premisecitation
Super-resolution microscopy has revealed sub-compartments inside DNA damage foci.
“In fact, sub-compartments within DNA damage foci have been observed by super-resolution microscopy, and their chromatin environments proposed to be distinct (Chapman et al., 2012).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Chapman et al., 2012 source
Not checked in the free run.
- The quote only partly states this claim. 2
- May combine two claims. 24
- Classified as probably not a substantial claim. 3
The quote only partly states this claim.
Findingown dataInterfering with chromatin condensation at damage sites (by tethering ASH2 to expand chromatin) reduces γ-H2AX and 53BP1 accumulation at I-SceI-induced breaks, despite higher DSB levels.
“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.”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Soutoglou et al., 2007 source
Not checked in the free run.
- Also stated in: § Chromatin condensation is an integral part of the DDR · plain
May combine two claims.
Findingown dataDNA damage causes chromatin at the damage site to first expand transiently, then compact and hypercondense beyond baseline.
“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.”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Kruhlak et al., 2006 source
Not checked in the free run.
- Also stated in: § Chromatin condensation is an integral part of the DDR · plain
May combine two claims.
Findingown dataDDR activation by chromatin condensation is not a cell cycle effect or due to stalled replication, as it occurs in cells arrested at G1/S or in G0.
“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”
Quote in the paperSubstantial claimMay combine two claims.
Findingown dataChromatin-induced DDR signaling requires both ATM and ATR; simultaneous depletion or inhibition reduces γ-H2AX to near background, while single ATM or ATR inhibition has modest effect and DNA-PK inhibition does not significantly reduce H2AX phosphorylation.
“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”
Quote in the paperSubstantial claim- Also stated in: § Condensed chromatin promotes activation of upstream parts of the DDR · plain
May combine two claims.
Findingown dataMitotic chromosomes, a naturally occurring condensed chromatin, show increased γ-H2AX (about 3-fold over interphase) and MDC1 foci, with 53BP1 excluded, in the absence of detectable DNA breaks.
“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”
Quote in the paperSubstantial claim0 of 2 sources checked- cites Ichijima et al., 2005 source
Not checked in the free run.
- cites McManus and Hendzel, 2005
Not checked in the free run.
- Also stated in: § Condensed chromatin activates upstream components of DDR signaling in mitotic cells · plain
May combine two claims.
Findingown dataTethering ASH2 to lacO arrays enriches H3K4me3 and expands chromatin.
“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”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Tumbar et al., 1999 source
Not checked in the free run.
- Also stated in: § Chromatin condensation is an integral part of the DDR · boosted
May combine two claims.
Findingown dataTethering HP1α, HP1β, HP1γ, or SUV3-9 to lacO arrays induces local chromatin compaction and H3K9me3 enrichment, with reduced nuclease accessibility.
“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”
Quote in the paperSubstantial claim0 of 3 sources checked- cites Danzer and Wallrath, 2004
Not checked in the free run.
- cites Li et al., 2003
Not checked in the free run.
- cites Verschure et al., 2005 source
Not checked in the free run.
- Also stated in: § Chromatin condensation triggers DDR signaling · plain
May combine two claims. The quote only partly states this claim.
Findingown dataTethering EZH2 to lacO arrays does not recruit DDR factors, unlike HP1 or SUV3-9.
“tethering of EZH2, a polycomb family protein involved in facultative heterochromatin formation, did not recruit DDR factors”
Quote in the paperSubstantial claimMay combine two claims.
Findingown dataChromatin condensation activates upstream DDR components but not downstream effectors; CHK2, SMC1, and p53 were not activated by HP1 tethering, and no cell cycle checkpoint activation was observed.
“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”
Quote in the paperSubstantial claim- Also stated in: § Condensed chromatin promotes activation of upstream parts of the DDR · boosted
May combine two claims.
Findingown dataGlobal chromatin compaction by SUV3-9 overexpression enhances early ATM signaling after γ-irradiation, shown by >2-fold increase in NBS1 phosphorylation and increased γ-H2AX.
“SUV3-9 overexpressing cells showed a greater than 2-fold increase in NBS1 phosphorylation, and increased γ-H2AX, suggesting enhanced early ATM signaling”
Quote in the paperSubstantial claim- Rests on an assumption: Overexpression of SUV3-9 globally compacts chromatin.
May combine two claims.
Findingown dataMDC1 and NBS1 are recruited to locally compacted chromatin domains, with 65-75% of arrays showing recruitment, a 2-fold increase over controls.
“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”
Quote in the paperSubstantial claim- Also stated in: § Condensed chromatin promotes activation of upstream parts of the DDR · plain
May combine two claims.
Findingown dataDDR activation by chromatin condensation is specific to condensed chromatin and not caused by arbitrary chromatin changes; tethering decondensation factors (ASH2, VP16, BRG1) does not autonomously recruit 53BP1 or induce γ-H2AX.
“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”
Quote in the paperSubstantial claim- Also stated in: § Chromatin condensation triggers DDR signaling · plain
May combine two claims.
Findingown dataBoth ATM and ATR contribute to mitotic chromatin-induced DDR, as caffeine treatment diminished pan-nuclear γ-H2AX levels more than ATM inhibition alone.
“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”
Quote in the paperSubstantial claimMay combine two claims.
Interpretationown dataHP1 does not act as a platform for DDR factor recruitment; condensed chromatin structures induce upstream DDR signaling.
“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.”
Quote in the paperSubstantial claimClassified as probably not a substantial claim. May combine two claims.
PremisecitationPhosphorylation enhances TIP60 acetyltransferase activity and can be induced by chromatin alterations, leading to ATM signaling independently of DNA breaks.
“phosphorylation enhances the acetyltransferase activity of TIP60, and this modification can be induced by chromatin alterations, leading to ATM signaling independently of DNA breaks”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Kaidi and Jackson, 2013 source
Not checked in the free run.
May combine two claims.
PremisecitationH3K9me3 stimulates binding and activation of TIP60 after DNA damage, which acetylates ATM and promotes its activation.
“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”
Quote in the paperSubstantial claim0 of 2 sources checked- Also stated in: § Introduction · plain
May combine two claims.
PremisecitationChromatin decondensation and histone reorganization occur after DSB induction and expedite downstream DDR.
“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”
Quote in the paperSubstantial claim0 of 3 sources checked- Also stated in: § Introduction · plain
May combine two claims.
PremisecitationHP1 tethering to lacO induces chromatin compaction and silencing.
“HP1 tethering to lacO has been previously shown to induce chromatin compaction and silencing”
Quote in the paperSubstantial claim0 of 3 sources checked- cites Danzer and Wallrath, 2004
Not checked in the free run.
- cites Li et al., 2003
Not checked in the free run.
- cites Verschure et al., 2005 source
Not checked in the free run.
May combine two claims.
Interpretationown dataCondensed chromatin domains are sufficient to trigger ATM/ATR-dependent signaling and activate upstream, but not downstream, components of the DDR cascade.
“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.”
Quote in the paperSubstantial claimMay combine two claims.
Interpretationown dataChromatin compaction enhances upstream DDR signaling but impairs repair and recovery from DNA damage.
“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”
Quote in the paperSubstantial claim- Also stated in: § Discussion · plain
Classified as probably not a substantial claim.
PremisecitationA transient repressive chromatin domain enriched in H3K9me2/3 is established at DNA damage sites by PRDM2 and SUV3-9.
“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”
Quote in the paperSubstantial claim0 of 2 sources checkedMay combine two claims.
PremisecitationSUV3-9 is recruited to double-strand breaks, where it establishes the repressive H3K9me3 mark, captures HP1, KAP-1 and more SUV3-9, and spreads heterochromatin for tens of kilobases around the break.
“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).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Ayrapetov et al., 2014 source
Not checked in the free run.
May combine two claims.
Interpretationown dataActivating DDR signaling involves chromatin condensation as a core step that is transient.
“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.”
Quote in the paperSubstantial claimMay combine two claims.
PremisecitationThe H3K9me3 repressive mark creates binding sites for TIP60 acetyltransferase, which contributes to amplifying ATM activity.
“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).”
Quote in the paperSubstantial claim0 of 3 sources checkedMay combine two claims.
PremisecitationATM signaling phosphorylates KAP-1 and releases the KAP-1/HP1/SUV3-9 and CHD3 complexes, which relaxes chromatin and is necessary for downstream signaling and repair.
“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).”
Quote in the paperSubstantial claim0 of 3 sources checkedProbably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.
PremisecitationATM kinase is activated within seconds after a double-strand break, and only a few strand breaks activate most of the large cellular ATM pool.
“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).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Bakkenist and Kastan, 2003 source
Not checked in the free run.
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?
(Epi)genomic context influences how efficiently DSBs are repaired.
“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]
DSBs are known to trigger dynamic reorganization of chromatin near breaks, which can affect expression of both nearby and apparently undamaged genes.
“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).”
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 · see citing works
RetractedThe ENCODE Project Consortium (2007) · Nature · doi:10.1038/nature05874 · Cited by 5,223 · see citing works
The DNA Damage Response: Making It Safe to Play with Knives
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DNA damage activates ATM through intermolecular autophosphorylation and dimer dissociation
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“Somewhat paradoxically, proteins that promote chromatin compaction, such as HP1, KAP-1, SPOC1, su(var)3-9 methyltransferase variant 1 (SUV3-9), PDRM2 methyltransferase, macro H2A, and histone deacetylases (HDACs), have also been shown to be recruited to the sites of DSBs (Ayoub et al., 2009; Ayrapetov et al., 2014; Ba…”
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- 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
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