Nanostructure of Clustered DNA Damage in Leukocytes after In-Solution Irradiation with the Alpha Emitter Ra-223.

DNA repair DSB focus substructure Single Molecule Localization Microscopy (SMLM) complex DNA damage high LET irradiation

Journal

Cancers
ISSN: 2072-6694
Titre abrégé: Cancers (Basel)
Pays: Switzerland
ID NLM: 101526829

Informations de publication

Date de publication:
26 Nov 2019
Historique:
received: 01 10 2019
revised: 22 11 2019
accepted: 23 11 2019
entrez: 30 11 2019
pubmed: 30 11 2019
medline: 30 11 2019
Statut: epublish

Résumé

Cancer patients are increasingly treated with alpha-particle-emitting radiopharmaceuticals. At the subcellular level, alpha particles induce densely spaced ionizations and molecular damage. Induction of DNA lesions, especially clustered DNA double-strand breaks (DSBs), threatens a cell's survival. Currently, it is under debate to what extent the spatial topology of the damaged chromatin regions and the repair protein arrangements are contributing. Super-resolution light microscopy (SMLM) in combination with cluster analysis of single molecule signal-point density regions of DSB repair markers was applied to investigate the nano-structure of DNA damage foci tracks of Ra-223 in-solution irradiated leukocytes. Alpha-damaged chromatin tracks were efficiently outlined by γ-H2AX that formed large (super) foci composed of numerous 60-80 nm-sized nano-foci. Alpha damage tracks contained 60-70% of all γ-H2AX point signals in a nucleus, while less than 30% of 53BP1, MRE11 or p-ATM signals were located inside γ-H2AX damage tracks. MRE11 and p-ATM protein fluorescent tags formed focal nano-clusters of about 20 nm peak size. There were, on average, 12 (± 9) MRE11 nanoclusters in a typical γ-H2AX-marked alpha track, suggesting a minimal number of MRE11-processed DSBs per track. Our SMLM data suggest regularly arranged nano-structures during DNA repair in the damaged chromatin domain.

Sections du résumé

BACKGROUND BACKGROUND
Cancer patients are increasingly treated with alpha-particle-emitting radiopharmaceuticals. At the subcellular level, alpha particles induce densely spaced ionizations and molecular damage. Induction of DNA lesions, especially clustered DNA double-strand breaks (DSBs), threatens a cell's survival. Currently, it is under debate to what extent the spatial topology of the damaged chromatin regions and the repair protein arrangements are contributing.
METHODS METHODS
Super-resolution light microscopy (SMLM) in combination with cluster analysis of single molecule signal-point density regions of DSB repair markers was applied to investigate the nano-structure of DNA damage foci tracks of Ra-223 in-solution irradiated leukocytes.
RESULTS RESULTS
Alpha-damaged chromatin tracks were efficiently outlined by γ-H2AX that formed large (super) foci composed of numerous 60-80 nm-sized nano-foci. Alpha damage tracks contained 60-70% of all γ-H2AX point signals in a nucleus, while less than 30% of 53BP1, MRE11 or p-ATM signals were located inside γ-H2AX damage tracks. MRE11 and p-ATM protein fluorescent tags formed focal nano-clusters of about 20 nm peak size. There were, on average, 12 (± 9) MRE11 nanoclusters in a typical γ-H2AX-marked alpha track, suggesting a minimal number of MRE11-processed DSBs per track. Our SMLM data suggest regularly arranged nano-structures during DNA repair in the damaged chromatin domain.

Identifiants

pubmed: 31779276
pii: cancers11121877
doi: 10.3390/cancers11121877
pmc: PMC6966434
pii:
doi:

Types de publication

Journal Article

Langues

eng

Subventions

Organisme : Deutsche Forschungsgemeinschaft
ID : SCHE350/12-2
Organisme : Deutsche Forschungsgemeinschaft
ID : LA 2304/3-2

Déclaration de conflit d'intérêts

The authors declare no conflict of interest. The funding sponsors had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript, and in the decision to publish the results.

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Auteurs

Harry Scherthan (H)

Bundeswehr Institute of Radiobiology affil. to the Univ. of Ulm, Neuherbergstraße 11, 80937 München, Germany.

Jin-Ho Lee (JH)

Bundeswehr Institute of Radiobiology affil. to the Univ. of Ulm, Neuherbergstraße 11, 80937 München, Germany.
Kirchhoff-Institute for Physics, Heidelberg University, Im Neuenheimer Feld 227, 69120 Heidelberg, Germany.

Emanuel Maus (E)

Bundeswehr Institute of Radiobiology affil. to the Univ. of Ulm, Neuherbergstraße 11, 80937 München, Germany.
Kirchhoff-Institute for Physics, Heidelberg University, Im Neuenheimer Feld 227, 69120 Heidelberg, Germany.

Sarah Schumann (S)

Dept. of Nuclear Medicine, Univ. of Würzburg, Oberdürrbacher Str. 6, 97080 Würzburg, Germany.

Razan Muhtadi (R)

Bundeswehr Institute of Radiobiology affil. to the Univ. of Ulm, Neuherbergstraße 11, 80937 München, Germany.

Robert Chojowski (R)

Kirchhoff-Institute for Physics, Heidelberg University, Im Neuenheimer Feld 227, 69120 Heidelberg, Germany.

Matthias Port (M)

Bundeswehr Institute of Radiobiology affil. to the Univ. of Ulm, Neuherbergstraße 11, 80937 München, Germany.

Michael Lassmann (M)

Dept. of Nuclear Medicine, Univ. of Würzburg, Oberdürrbacher Str. 6, 97080 Würzburg, Germany.

Felix Bestvater (F)

German Cancer Research Center (DKFZ), Im Neuenheimer Feld 280, 69120 Heidelberg, Germany.

Michael Hausmann (M)

Kirchhoff-Institute for Physics, Heidelberg University, Im Neuenheimer Feld 227, 69120 Heidelberg, Germany.

Classifications MeSH