Associate Chair for Graduate Studies
Office: BMH 3031
Phone: 519-888-4567, ext. 38131
The primary focus of my research program (The Muscle Biology & Cell Death Laboratory) is to study the biochemical and molecular mechanisms regulating cell death processes (i.e., autophagy and apoptosis) in skeletal muscle. Apoptosis is a highly conserved cell death mechanism that allows multi-cellular organisms to maintain tissue and cellular homeostasis. Autophagy is a cellular degradation process that aids in the removal of cytoplasmic contents such as macromolecules and organelles, that also influences tissue function and cell death. A wealth of literature has established dysregulation of autophagy and apoptosis as key mechanisms in the pathogenesis of disease. In skeletal muscle, apoptosis and autophagy dramatically influence normal tissue development, but also tissue wasting and dysfunction.
The Muscle Biology & Cell Death Laboratory is at the forefront of understanding the role of autophagic signaling in the formation and maintenance of skeletal muscle. We recently discovered that autophagy and a specialized type of autophagy that degrades mitochondria (mitophagy) are required for skeletal muscle differentiation. Importantly, autophagy and mitophagy protect muscle cells during the differentiation process by preventing mitochondrial-mediated oxidative stress and cell death events. In addition, autophagy/mitophagy influence mitochondrial biogenesis as well as fission and fusion processes that ultimately impact mitochondrial quality control and network remodelling in skeletal muscle. New work in our lab is also examining the influence of autophagy on satellite cell function and skeletal muscle regeneration, as well as the role of autophagic signaling on skeletal muscle morphology, adaptation, and function.
The Muscle Biology & Cell Death Laboratory is also defining some of the important differences in apoptotic signaling and susceptibility between muscles, fiber types, and mitochondria. We are also investigating the critical role of oxidative stress, mitochondrial content/function, and mitochondrial fission/fusion processes on apoptotic susceptibility. Not only are we studying the detrimental effects of apoptotic signaling in skeletal muscle, but we are defining key signaling aspects that are essential in skeletal muscle differentiation and formation. For example, our lab recently discovered that caspase-2 plays an indispensable role in skeletal muscle myogenesis.
Physical activity plays an important role in the management and prevention of disease. Exercise can alter a number of intracellular and extracellular signaling pathways. New research from the Muscle Biology & Cell Death Laboratory has also found that exercise can influence autophagic and apoptotic signaling in skeletal muscle. In particular, regular physical activity can promote a “pro-survival” environment in skeletal muscle. Collectively, the evidence suggests that lifestyle modifications may preserve cellular function during aging and disease by altering autophagy and apoptotic signaling processes.
For further information please visit the Muscle Biology & Cell Death Laboratory website.
Graduate supervision and student opportunities
I am currently accepting applications for student opportunities in the following areas:
- Research volunteer
- Undergraduate thesis
- MSc thesis
- PhD thesis
- Postdoctoral fellowship
Please email me to discuss current available opportunities.
Teaching, expertise, tools and technologies
- Skeletal muscle biology
- Skeletal muscle disease
- Exercise physiology
- Cell and molecular biology
- Cell culture
- Animal models
- Cellular imaging
KIN 406: Physiology of Skeletal Muscle Aging & Disease
KIN 606: Molecular Basis of Disease
Bloemberg, D. and Quadrilatero J. Autophagy, apoptosis, and mitochondria: Molecular integration and physiological relevance in skeletal muscle. American Journal of Physiology – Cell Physiology (In Press).
Baechler, B.L., Bloemberg, D., Quadrilatero, J. Mitophagy regulates mitochondrial network signaling, oxidative stress, and apoptosis during myoblast differentiation. Autophagy (In Press).
Boonstra, K., Bloemberg, D., Quadrilatero, J. Caspase-2 is required for skeletal muscle differentiation and myogenesis. Biochimica et Biophysica Acta (BBA) - Molecular Cell Research, 2018, 1865: 95-104.
Vorobej, K., Mitchell, A.S., Smith, I.C., Donath, S., Tupling A.R., Quadrilatero, J. The effect of ARC ablation on skeletal muscle morphology, function, and apoptotic signaling during aging. Experimental Gerontology 2018, 101: 69-79.
Paré, M-F., Baechler, B.L., Fajardo, V.A., Earl, E., Wong, E., Campbell, T.L., Tupling, A.R., Quadrilatero, J. Effect of acute and chronic autophagy deficiency on skeletal muscle apoptotic signaling, morphology, and function. Biochimica et Biophysica Acta (BBA) - Molecular Cell Research, 2017, 1864: 708-718.
McMillan, E.M., Paré, M-F., Baechler B.L., Graham, D.A., Rush, J.W.E., Quadrilatero, J. Autophagic signaling and proteolytic enzyme activity in cardiac and skeletal muscle of spontaneously hypertensive rats following chronic aerobic exercise. PLoS ONE, 2015, 10: e0119382.
Mitchell, A.S., Smith, I.C., Gamu, D., Donath, S., Tupling, A.R., Quadrilatero, J. Functional, morphological, and apoptotic alterations in skeletal muscle of ARC deficient Mice. Apoptosis, 2015, 20: 310-326.
Campbell, T.L., Mitchell, A.S., McMillan, E.M., Bloemberg, D., Pavlov, D., Messa, I., Mielke, J.G., Quadrilatero, J. Effect of a 16 week high fat diet on rat skeletal muscle autophagic and apoptotic signaling. Experimental Biology and Medicine, 2015, 240: 657-668.
Bloemberg, D. and Quadrilatero, J. Mitochondrial pro-apoptotic indices do not precede the transient caspase activation associated with myogenesis. Biochimica et Biophysica Acta - Molecular Cell Research, 2014, 1843: 2926-2936.
McMillan, E.M. and Quadrilatero, J. Autophagy is required and protects against apoptosis during myoblast differentiation. Biochemical Journal, 2014, 462: 267-277.
Bloemberg, D. and Quadrilatero, J. Rapid determination of myosin heavy chain expression in rat, mouse, and human skeletal muscle using multicolor immunofluorescence analysis. PLoS ONE, 2012, 7: e35273.
Quadrilatero, J., Alway, S.E., Dupont-Versteegden, E.E. Skeletal muscle apoptotic response to physical activity: Potential mechanisms for protection. Applied Physiology, Nutrition, and Metabolism, 2011, 36: 608-617.