The D’Amours laboratory is currently recruiting graduate students and post-doctoral fellows. Please send your CV to:
When Damien D’Amours began his doctoral studies at the University of Cambridge in 1997, he was specifically interested in Nijmegen breakage syndrome (NBS), a childhood disease that affects DNA repair and checkpoint mechanisms. During his doctoral studies, he investigated the specific cause of this disease, a dysfunction in the activity of the Mre11 complex. His research showed that the nuclear monitoring function of the Mre11 complex is vital for the maintenance of genomic integrity and the inability to perform this function is a likely cause for the high cancer rates in NBS patients.
He then moved to the Massachusetts Institute of Technology (MIT) in Boston to conduct postdoctoral studies. He was awarded the prestigious Damon Runyon Postdoctoral Fellowship from the Damon Runyon Cancer Research Foundation (2003-2005) to accomplish this phase of his career. His work led to the discovery of an essential and completely novel genome segregation mechanism acting during cell division. He also found that an intracellular signaling network called FEAR (for Cdc fourteen-early anaphase release) network plays a key role in the separation of chromosomes to daughter cells during mitosis.
After eight years away from Canada, Damien D’Amours returned in 2005 to begin work as a principal investigator and professor at IRIC/Université de Montréal. He received the Canada Research Chair in Cell Cycle Regulation and Genomic Integrity, & a Senior Scholar Award from FRQ-S for this phase of his career. After twelve years in Montréal, Dr. D’Amours was recruited at the University of Ottawa in 2017 where he aims to decipher the molecular pathways responsible for the maintenance of genome integrity in living cells.
Damien D’Amours and his team study the mechanisms that regulate cell division and genome stability in eukaryotes. In particular, his research aims to shed light on how cells divide their genome during proliferation and how they repair their chromosomes in the presence of DNA damage. The aim of his research is to foster the development of drugs that limit the ability of cancer cells to multiply uncontrollably during tumor formation. To achieve this aim, a team of dedicated graduate students and post-doctoral fellows in Dr. D’Amours’ laboratory are using a multidisciplinary approach together with cutting edge techniques and national/international collaborations to reveal core mechanisms that drive the cell cycle in normal and pathological conditions.
- Role of polo kinases in checkpoint adaptation after DNA damage
- Proteome-wide mass spectrometry analysis of phosphorylation dynamics during the cell cycle
- The LICS syndrome: Roles of the Smc5-6 complex in DNA repair and genome integrity
- Regulation of chromosome morphogenesis during cell division
Genetics, live cell microscopy, cell cycle analyses, chromatin imaging, proteomics, characterization of post-translational modifications, protein purification, biophysics, systems biology, model organisms, yeast.
- Serrano D, D’Amours D. Checkpoint adaptation: Keeping Cdc5 in the T-loop. Cell Cycle. 2016; 15: 3339-3340.
- Ratsima, H, Serrano, D, Pascariu, M, D’Amours D. Centrosome-dependent bypass of the DNA damage checkpoint by the Polo kinase Cdc5. Cell Reports 2016; 14: 1422-1434.
- Robellet X, Thattikota Y, Wang F, Wee TL, Pascariu M, Shankar S, Bonneil É, Brown CM, D’Amours D. A high-sensitivity phospho-switch triggered by Cdk1 governs chromosome morphogenesis during cell division. Genes & Development 2015; 29: 426-439.
- Roy M-A, Dhanaraman T, D’Amours, D. The Smc5-Smc6 heterodimer associates with DNA through several independent binding domains. Scientific Reports 2015; 5: 9797.
- Walters AD, May CK, Dauster ES, Cinquin BP, Smith EA, Robellet X, D’Amours D, Larabell CA, Cohen-Fix O. The yeast polo kinase Cdc5 regulates the shape of the mitotic nucleus. Current Biology 2014; 24: 2861-2867.
- Ratsima H, Ladouceur A-M, Pascariu M, Sauvé V, Salloum Z, Maddox PS, D’Amours D. Independent modulation of the kinase and polo-box activities of Cdc5 protein unravels unique roles in the maintenance of genome stability. Proceedings of the National Academy of Sciences USA 2011; 108: E914-E923.à
- St-Pierre J, Douziech M, Bazile F, Pascariu M, Bonneil E, Sauvé V, Ratsima H, D’Amours D. Polo kinase regulates mitotic chromosome condensation by hyperactivation of condensin DNA supercoiling activity. Molecular Cell 2009; 34: 416-426.
- D'Amours D, Stegmeier F, Amon A. Cdc14 and condensin control the dissolution of cohesin-independent chromosome linkages at repeated DNA. Cell 2004; 117: 455-469.
- Goldberg M, Stucki M, Falck J, D'Amours D, Rahman D, Pappin D, Bartek J, Jackson SP. MDC1 is required for the intra-S-phase DNA damage checkpoint. Nature 2003; 421: 952 –956.
- D'Amours D, Jackson SP. The Mre11 complex: At the crossroads of DNA repair and checkpoint signalling. Nature Reviews in Molecular Cell Biology 2002; 3: 317-327.