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Detail

Joanna Loizou
Dr Joanna Loizou, PhDPrincipal Investigator at CeMM

CeMM, external institution
Position: Associate Professor

ORCID: 0000-0003-1853-0424
T +43 1 40160 70058
jloizou@cemm.oeaw.ac.at

Further Information

Keywords

CRISPR-Cas Systems; DNA Breaks; DNA Repair

Research group(s)

  • Joanna Loizou
    Research Area: The human genome is constantly exposed to endogenous and exogenous sources of DNA damage. DNA repair ensures the integrity of large eukaryotic genomes. We are interested in exploring the DNA repair pathways that maintain genome stability.
    Members:

Research interests

The human genome is constantly exposed to endogenous and exogenous sources of DNA damage. DNA repair ensures the integrity of large eukaryotic genomes by minimising the mutation rate. We are interested in exploring the several highly effective pathways for DNA repair that have distinct specificities, and are evolutionary conserved despite partial redundancies. While somatic defects in DNA repair genes contribute to cancer and other severe diseases, germline mutations in relevant DNA repair genes cause specific deficiencies which are the underlying cause for a family of rare diseases. We are investigating the genetic interactions of the intricate crosstalk between DNA damage and repair mechanisms with the ultimate goal that this may pave the way to rational therapeutic approaches. Our three main focus areas are:

  1. Consequences of DNA damage and repair on genomic mutation signatures
  2. Synthetic lethal and viable interactions
  3. Repair of CRISPR-Cas9 generated DNA breaks

The successful implementation of the above outlined research proposal will constitute a significant contribution to the field of DNA repair and the diseases caused by defects in these pathways.

Techniques, methods & infrastructure

My team investigates the cellular pathways that respond to DNA damage, to maintain genome stability and suppress cancer development. Our goal is to piece together the intricate puzzle that encompasses the human DNA damage response at the cellular level, hence providing a complete understanding of how such pathways go wrong in disease states, with a strong emphasis on cancer. To achieve this, we use global approaches, based around genetics, genomics, proteomics and chemical biology.

Grants

  • Mapping Mutation signatures that occur due to defects in DNA repair (2019)
    Source of Funding: City of Vienna, City of Vienna Prize
    Principal Investigator
  • REAP-Repair of DNA lesions induced by platinum drugs (2019)
    Source of Funding: EU, MSCA
    Principal Investigator
  • MUTYH: better without? Seeking fundamental insights into the clearance of UV-induced DNA damage by loss of MUTYH (2018)
    Source of Funding: OeAW (Austrian Academy of Sciences), DOC Fellowship
    Principal Investigator
  • Exploiting novel interactions between cancer-associated kinases and DNA damage-inducing chemotherapeutics (2016)
    Source of Funding: FWF (Austrian Science Fund), Stand Alone
    Principal Investigator
  • Synthetic rescue to correct rare diseases associated with defective nucleotide excision repair (2016)
    Source of Funding: FWF (Austrian Science Fund), Stand Alone
    Principal Investigator

Selected publications

  1. Owusu, M. et al., 2019. Mapping the Human Kinome in Response to DNA Damage. Cell Reports, 26(3), pp.555–563.e6. Available at: http://dx.doi.org/10.1016/j.celrep.2018.12.087.
  2. Velimezi, G. et al., 2018. Map of synthetic rescue interactions for the Fanconi anemia DNA repair pathway identifies USP48. Nature Communications, 9(1). Available at: http://dx.doi.org/10.1038/s41467-018-04649-z.
  3. Zou, X. et al., 2018. Validating the concept of mutational signatures with isogenic cell models. Nature Communications, 9(1). Available at: http://dx.doi.org/10.1038/s41467-018-04052-8.
  4. Mazouzi, A. et al., 2017. Repair of UV-Induced DNA Damage Independent of Nucleotide Excision Repair Is Masked by MUTYH. Molecular Cell, 68(4), pp.797–807.e7. Available at: http://dx.doi.org/10.1016/j.molcel.2017.10.021.
  5. Moder, M. et al., 2017. Parallel genome-wide screens identify synthetic viable interactions between the BLM helicase complex and Fanconi anemia. Nature Communications, 8(1). Available at: http://dx.doi.org/10.1038/s41467-017-01439-x.