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BIOspektrum

, 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
  • 13 Downloads

Abstract

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.

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Literatur

  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

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