- Functional interplay between the oxidative stress response and DNA damage checkpoint signaling for genome maintenance in aerobic organisms
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Ji Eun Choi , Woo-Hyun Chung
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J. Microbiol. 2020;58(2):81-91. Published online December 23, 2019
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DOI: https://doi.org/10.1007/s12275-020-9520-x
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The DNA damage checkpoint signaling pathway is a highly
conserved surveillance mechanism that ensures genome integrity
by sequential activation of protein kinase cascades.
In mammals, the main pathway is orchestrated by two central
sensor kinases, ATM and ATR, that are activated in response
to DNA damage and DNA replication stress. Patients
lacking functional ATM or ATR suffer from ataxia-telangiectasia
(A-T) or Seckel syndrome, respectively, with pleiotropic
degenerative phenotypes. In addition to DNA strand
breaks, ATM and ATR also respond to oxidative DNA damage
and reactive oxygen species (ROS), suggesting an unconventional
function as regulators of intracellular redox status.
Here, we summarize the multiple roles of ATM and ATR, and
of their orthologs in Saccharomyces cerevisiae, Tel1 and Mec1,
in DNA damage checkpoint signaling and the oxidative stress
response, and discuss emerging ideas regarding the possible
mechanisms underlying the elaborate crosstalk between those
pathways. This review may provide new insights into the integrated
cellular strategies responsible for maintaining genome
stability in eukaryotes with a focus on the yeast model
organism.
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Citations
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- Synthetic lethal interaction between oxidative stress response and DNA damage repair in the budding yeast and its application to targeted anticancer therapy
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Ji Eun Choi , Woo-Hyun Chung
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J. Microbiol. 2019;57(1):9-17. Published online December 29, 2018
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DOI: https://doi.org/10.1007/s12275-019-8475-2
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Synthetic lethality is an extreme form of negative genetic
epistasis that arises when a combination of functional deficiency
in two or more genes results in cell death, whereas none
of the single genetic perturbations are lethal by themselves.
This unconventional genetic interaction is a modification
of the concept of essentiality that can be exploited for the
purpose of targeted cancer therapy. The yeast Saccharomyces
cerevisiae has been pivotally used for early large-scale synthetic
lethal screens due to its experimental advantages, but
recent advances in gene silencing technology have now made
direct high-throughput analysis possible in higher organisms.
Identification of tumor-specific alterations and characterization
of the mechanistic principles underlying synthetic lethal
interaction are the key to applying synthetic lethality to clinical
cancer treatment by enabling genome-driven oncological
research. Here, we provide emerging ideas on the synthetic
lethal interactions in budding yeast, particularly between cellular
processes responsible for oxidative stress response and
DNA damage repair, and discuss how they can be appropriately
utilized for context-dependent cancer therapeutics.
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