Dr. Gordon L. Rintoul

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Dr. Gordon L. Rintoul Assistant Professor CIHR New Investigator in the Area of Aging
	B.Sc., University of Western Ontario, Ph.D., UBC

	Office:	778-782-4801	Room B8224
	Lab:	778-782-7340	Room B9226, 9218
	gordon_rintoul@sfu.ca		Contact Us
	Selected Publications		Prospective Students

Current Research Program:

The Hidden Life of Mitochondria

The image of the mitochondrion presented in most text books is that of a static, sausage-shaped "power house of the cell". While it is true that the primary function of mitochondria is the generation of ATP to power most cellular functions, recent research has revealed that mitochondria are (literally) much more multi-dimensional. Mitochondria are very polymorphic and dynamic organelles. While some mitochondria do possess a tubular shape, some are much more rounded, and in some cells mitochondria form a continuous web-like network. Perhaps one of the more surprising and interesting aspects of mitochondria is that they are dynamic organelles: they undergo fusion, fission, and they are rapidly transported throughout the cell. The term “Mitochondrial Homeostasis” has been used to describe the amalgam of all the processes which influence the number, shape and position of mitochondria. These include mitochondrial biogenesis, fission, fusion, transport and degradation. The cellular control, mechanics and in some cases even the significance of these processes are poorly understood. To study these processes, I employ targeted expression of fluorescent proteins which allows for examination of individual mitochondria within cells using fluorescence microscopy (see micrographs below).

Mitochondria and Neuronal Injury

The dysfunction of mitochondria has been implicated in many progressive neurodegenerative disorders and more acute ischemic cell death. One of the major themes of my research is the role of mitochondria in cell death, examining modulation of intracellular calcium, disruption of ATP generation, and release of factors from mitochondria which participate in cell death mechanisms.

The impact of the physiologic (ATP generation & calcium buffering) and pathophysiologic (release of pro-apoptotic proteins and reactive oxygen species) functions of mitochondria may be critically affected by changes in mitochondrial homeostasis. Therefore my guiding hypothesis is that normal biogenesis, fission, fusion, trafficking and degradation of mitochondria are essential for neuronal function and disruption of mitochondrial homeostasis is a factor in neuronal injury mechanisms.

      Below: Fluorescence micrographs (low and high magnification) of a
      neuron co-transfected with mitochondrially-targeted yellow fluorescent protein
      and cytoplasmic cyan fluorescent protein.

Positions Available:

Please contact me at the email address listed above to discuss the possibility of joining my lab. Prospective graduate students should also click the following link for information on the graduate program in Biological Sciences.