, Volume 24, Issue 3, pp 269–272 | Cite as

High-content imaging für multidimensionale Zellanalysen

  • Aleksandra Lezaja
  • Matthias Altmeyer
Wissenschaft · Special: High Content Imaging Mikroskopiebasierte Zytometrie


Automated high-throughput microscopy has been instrumental for drug discovery and large-scale gene perturbation screens. Advancements in image resolution, microscope speed, and detection sensitivity have greatly aided high-content imaging approaches. Here, we describe how high-content microscopy can be repurposed for quantitative image-based cytometry, an approach that exploits both the throughput and the resolution of current screening microscopes for multidimensional cell population analyses.


Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.


  1. [1]
    Altmeyer M, Toledo L, Gudjonsson T et al. (2013) The chromatin scaffold protein SAFB1 renders chromatin permissive for DNA damage signaling. Mol Cell 52:206–220CrossRefPubMedGoogle Scholar
  2. [2]
    Ochs F, Somyajit K, Altmeyer M et al. (2016) 53BP1 fosters fidelity of homology-directed DNA repair. Nat Struct Mol Biol 23:714–721CrossRefPubMedGoogle Scholar
  3. [3]
    Pellegrino S, Michelena J, Teloni F et al. (2017) Replication-coupled dilution of H4K20me2 guides 53BP1 to pre-replicative chromatin. Cell Rep 19:1819–1831CrossRefPubMedPubMedCentralGoogle Scholar
  4. [4]
    Toledo LI, Altmeyer M, Rask MB et al. (2013) ATR prohibits replication catastrophe by preventing global exhaustion of RPA. Cell 155:1088–1103CrossRefPubMedGoogle Scholar
  5. [5]
    Lukas J, Lukas C, Bartek J (2011) More than just a focus: the chromatin response to DNA damage and its role in genome integrity maintenance. Nat Cell Biol 13:1161–1169CrossRefPubMedGoogle Scholar
  6. [6]
    Mankouri HW, Huttner D, Hickson ID (2013) How unfinished business from S-phase affects mitosis and beyond. EMBO J 32:2661–2671CrossRefPubMedPubMedCentralGoogle Scholar
  7. [7]
    Lezaja A, Altmeyer M (2017) Inherited DNA lesions determine G1 duration in the next cell cycle. Cell Cycle 17:24–32CrossRefPubMedPubMedCentralGoogle Scholar
  8. [8]
    Arora M, Moser J, Phadke H et al. (2017) Endogenous replication stress in mother cells leads to quiescence of daughter cells. Cell Rep 19:1351–1364CrossRefPubMedPubMedCentralGoogle Scholar
  9. [9]
    Barr AR, Cooper S, Heldt FS et al. (2017) DNA damage during S-phase mediates the proliferation-quiescence decision in the subsequent G1 via p21 expression. Nat Commun 8:14728CrossRefPubMedPubMedCentralGoogle Scholar
  10. [10]
    Yang HW, Chung M, Kudo T et al. (2017) Competing memories of mitogen and p53 signalling control cell-cycle entry. Nature 549:404–408CrossRefPubMedGoogle Scholar
  11. [11]
    Spencer SL, Cappell SD, Tsai FC et al. (2013) The proliferation-quiescence decision is controlled by a bifurcation in CDK2 activity at mitotic exit. Cell 155:369–383CrossRefPubMedPubMedCentralGoogle Scholar
  12. [12]
    Strauss R, Bartek J (2018) Daughters sense their mother’s stress. Cell Cycle 17:145–146CrossRefPubMedGoogle Scholar

Copyright information

© Springer-Verlag GmbH Deutschland, ein Teil von Springer Nature 2018

Authors and Affiliations

  1. 1.Department of Molecular Mechanisms of DiseaseUniversität ZürichZürichSchweiz
  2. 2.Cancer Biology Program, Life Science Zurich Graduate SchoolUniversität ZürichZürichSchweiz

Personalised recommendations