Hugh P. J. Bennett

Picture of HPJB


Hugh P.J. Bennett, Ph.D.

Professor, Department of Medicine

Metabolic Diseases and Complications Program

Centre for Translational Biology
Research Institute of the McGill University Health Centre 

EM2.3226 (office) EM1.3229 (mail drop)

1001 Decarie Blvd.
Montreal, QC H4A 3J1

Tel: 514-934-1934 ext. 76390

hugh.bennett [at]


Biographical Sketch

Professor, McGill University, 1993-
Associate Professor, McGill University, 1986-1993
Assistant Professor, McGill University, 1980-1986
Medical Scientist, Department of Medicine, Royal Victoria Hospital, Montreal, 1980-
Post-Doctoral Fellow, McGill University, 1978-1980
External Post Graduate Research Student, Brunel University, 1973-1977

Canadian Pacific Professor of Biotechnology, 2004-2009

Director: Division of Experimental Medicine of Faculty of Medicine, 2003 – 2013
Director: Sheldon Biotechnology Centre of McGill University, 1992 - 2012.
Director: Endocrine Laboratory, Royal Victoria Hospital, 1995 - 2005


Zebrafish, progranulin, motor neuron development, in situ hybridization, protein structure, chromatography

Research or Clinical Activities

The zebrafish has emerged as a model organism that is expected to define the mechanisms underlying the development of functions unique to vertebrates including humans (i.e. the heart, blood vessels, and advanced nervous and immune systems). We are using the Zebrafish to study the function of a new family of tissue growth factors (the granulins) discovered in the Endocrine Laboratory. In mammals, over-expression of the single granulin gene has been shown to contribute to the progression of certain tumours including those of the breast and prostate. In contrast granulin gene under-expression resulting from the loss of one allele has been shown to lead to a form of frontotemporal dementia in human patients. We have shown that in the zebrafish, the granulins are members of a multi-gene family that are critically involved in early embryonic development. Knockdown of granulin gene expression leads to a profound disruption of organ formation including interference in normal development of the central nervous system, internal organs, blood cells and blood vessels. One of the more tractable consequences of knockdown of pgrna in Zebrafish is disruption of normal caudal motor neuron development. We are using this developmental assay to define the mechanism of action of progranulin and applying this knowledge to the development of model therapeutics with potential for treating chronic neurological diseases.

Selected Recent Publications

Tauffenberger, A., Chitramuthu, B.P., Bateman, A., Bennett, H.P.J. and Parker, J.A. Reduction of polyglutamine toxicity by TDP-43, FUS and Progranulin in Huntington's Disease models.  Hum. Mol. Genet., 22, 782-794, 2013

Chitramuthu, B.P., and Bennett, H.P.J. Use of High Resolution Whole Mount In Situ Hybridization and Monitoring and Imaging In Vivo within Zebrafish Embryos to Study Gene Expression and Function. Journal of Visualised Experiments, 80, e50644, doi:10.3791/50644, 2013

Palfree R.G.E., Bennett H.P.J. and Bateman A. The Evolution of the Secreted Regulatory Protein Progranulin. PLoS One doi:10: e0133749, 2015

Chitramuthu B.P.., Kay, D.G., Bateman, A. and Bennett, H.P.J. Neurotrophic effects of PGRN in vivo in reversing motor neuron defects caused by over or under expression of TDP-43 or FUS. PLoS One.doi e0174784, 2017

Chitramuthu, B.P., Bennett H.P.J and Bateman A... Progranulin: a new avenue towards the understanding and treatment of neurodegenerative disease. Brain, doi:10. 1093/brain/awx198, 2017

See also Google Scholar

PubMed Publications - H Bennett

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