Why I Became a Scientist
What initially drove me to study biology was curiosity. Since I can remember, I always wanted to know “why” things were the way they were. As I advanced in my undergraduate studies, I felt more and more attracted to the field of genetics and molecular biology, as these disciplines seem to have the power to answer fundamental questions about living organisms and help understand and cure illnesses. I currently use molecular biology techniques to understand the first events that lead to the development of cancer.
DNA damage is the underlying cause of genomic instability that leads to cell transformation and the development of cancer. In response to DNA damage, eukaryotic cells trigger the activation of a complex series of pathways to allow repair of the damaged DNA. The activation of apoptosis (cell suicide) is also an essential component of the DNA damage response as it prevents cells with genomic alterations from proliferating to a malignant state. Thus, disruption of either mechanisms that control the repair of DNA lesions or the activation of apoptotic pathways results in genomic instability and contributes to the development of cancer.
My research program focuses on DNA repair/signaling pathways activated by double-stranded DNA breaks- one of the most dangerous forms of DNA damage – with a focus on understanding how DNA gets repaired, and how apoptosis is activated when repair is not completed.
How does RanBPM (Ran-binding protein M) functions to control the activation of apoptosis in response to DNA damage?
How does DNA repair factor Ku functions to repair and signal from a double-stranded DNA break?
- Undergraduate in Biology at the University of Lausanne, Switzerland (Major in Molecular Biology).
- Master and PhD at the University of Lausanne. Topic: Mechanisms regulating gene expression. - PhD training included a 2-year stage at the National Institutes of Health, Bethesda, USA.
- Posdoctoral Fellow at the Institut de Biologie Moléculaire et Cellulaire du CNRS, Strasbourg, France
- Postdoctoral Fellow at the Loeb Research Institute (now part of the Ottawa Health Research Inst – OHRI), Faculty of Medicine, University of Ottawa.
- Research Associate at the Ottawa Health Research Institute, Faculty of Medicine, University of Ottawa
- Natural Sciences and Engineering Research Council Canada (NSERC) Discovery Accelerator Award (DAS)
- Post-doctoral Fellowship, Medical Research Council of Canada and the Arthritis Society
- Post-doctoral Fellowship, Association pour la Recherche sur le Cancer (France)
- Fellowship, Centre National de la Recherche Scientifique (France)
- Post-doctoral Fellowship, Swiss National Science Foundation (Switzerland)
McTavish CJ, Berube-Janzen W, Maitland MER, Wang X, Salemi LM, Hess DA, Schild-Poulter C. (2019) Regulation of c-Raf stability through the CTLH complex. Int J Mol Sci 20(4):934.
Abbasi S and Schild-Poulter C. (2018) Mapping the Ku protein interactome using proximity-dependent biotin identification in human cells. J Proteome Res 18(3):1064-1077.
Salemi LM, Maitland MER, Yefet E, Schild-Poulter C. (2017) Inhibition of HDAC6 activity through interaction with the RanBPM-CTLH complex. BMC Cancer 17(1):460.
Salemi LM, Maitland MER, McTavish CJ, Schild-Poulter C. (2017) Cell signaling pathway reculation by RanBPM: molecular insights and disease implications. Open Biol 7(6): 170081.
Wolfs JM, Hamilton TA, Lant JT, Laforet M, Zhang J, Salemi LM, Gloor GB, Schild-Poulter C, and Edgell DR. (2016) Biasing genome-editing events towards precise length deletions with an RNA-guided TevCas9 dual nuclease. Proc Natl Acad Sci USA. 113(52):14988-14993.
Fell VL, Walden EA, Hoffer SM, Rogers SR, Aitken AS, Salemi LM, and Schild-Poulter C. (2016) Ku70 Serine 155 mediates Aurora B inhibition and activation of the DNA damage response. Sci Rep, 6, 37194.
Fell VL and Schild-Poulter C. (2015) The Ku heterodimer: function in DNA repair and beyond. Mutat Res Rev Mutat Res 763:15-29.
Salemi L, Loureiro S and Schild-Poulter C. (2015) Characterization RanBPM molecular determinants that control its subcellular localization. PLoS One 10(2):e0117655.
Wolfs JM, DaSilva M, Meister SE, Wang X, Schild-Poulter C and Edgell DR. (2014)
MegaTevs: single-chain dual nucleases for efficient gene disruption. Nucleic Acids Res 42(13):8816-8829.
Salemi L, Almazi A, Lefevbre K and Schild-Poulter C. (2014)
Aggresome formation is regulated by RanBPM through an interaction with HDAC6. Biol Open 3(6):418-430.
Kleinstiver BP, Wang L, Wolfs JA, Kolaczyk T, McDowell B, Wang X, Schild-Poulter C, Kumar S, Haerizadeh F, Bogdanove AJ and Edgell DR. (2014)
The I-Tevl nuclease and linker domains contribute to the specificity of monomeric TALENs. G3 (Bethesda) 4(6):1155-1165.
Soares IN, Caetano FA, Pinder J, Rodrigues BR, Beraldo FH, Ostapchenko VG, Durette C, Pereira GS, Lopes MH, Queiroz-Hazarbassanov N, Cunha IW, Sanematsu PI, Suzuki S, Bleggi-Torres LF, Schild-Poulter C, Thibault P, Dellaire G, Martins VR, Prado VF, Prado MA. (2013)
Regulation of stress-inducible phosphoprotein 1 nuclear retention by protein inhibitor of activated STAT PIAS1. Mol Cell Proteomics 12(11):3253-3270.
Atabakhsh E and Schild-Poulter C. (2012) RanBPM is an inhibitor of ERK signaling. PLoS One 7(10):e47803.
Zhurov V, Stead J, Merali Z, Palkovits M, Faludi G, Schild-Poulter C, Anisman H and Poulter MO. (2012)
Molecular pathway reconstruction and analysis of disturbed gene expression in depressed individuals who died by suicide. PLoS One 7(10):e47581.
Atabakhsh E, Wang JH Wang X, Carter DE and Schild-Poulter C. (2012) RanBPM expression regulates transcriptional pathways involved in development and tumorigenesis. Am J Cancer Res 2(5):549-565.
Fell VL and Schild-Poulter C. (2012) Ku regulates DNA damage signaling through the Ku70 N-terminal von Willebrand A domain. Mol Cell Biol 32(1):76-87.
Robarts Research Institute
Molecular Medicine: Vascular and Brain Health Group
1151 Richmond St. N.
London, Ontario, N6A 5B7
Phone: 519-663-5777 ext. 24164