Mathieu Laplante, PhD
Assistant Professor of Medicine
Mathieu Laplante was trained in the laboratory of Yves Deshaies at Laval University where he obtained
a PhD degree in 2007. The objective of his work was to improve the understanding of the mechanisms by which PPARg
agonists modulate white adipose tissue distribution. After getting his degree, he joined the laboratory of David M Sabatini
at the Whitehead Institute of Biomedical research, a research center affiliated to the Massachusetts Institute of Technology
(MIT) in Boston. From 2007 to 2011, he worked on the identification and the characterization of a new mTOR-interacting
protein named DEPTOR. In 2011, he was recruited as assistant Professor by the Department of Medicine at Laval University.
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Selected Scientific Contributions
1) Laplante M, Horvat S, et al., DEPTOR cell-autonomously promote adipogenesis and is
overexpressed in obesity. Cell Metab, 8;16(2):202-12, 2012.
In this paper, we identify DEP domain containing mTOR-interacting protein (DEPTOR) as a positive regulator of adipogenesis
that is associated with obesity. Using a doxycycline inducible mouse model for Deptor overexpression, we show that Deptor
promotes adipose tissue expansion in vivo. DEPTOR expression is elevated in adipose tissue of obese humans and strongly
correlates with the degree of obesity. We show that DEPTOR is induced during adipogenesis and that its overexpression
cell-autonomously promotes adipogenesis. These results establish DEPTOR as a physiological regulator of adipogenesis.
2) Peterson TR, Laplante M, et al., DEPTOR is an mTOR inhibitor frequently overexpressed
in multiple myeloma cells and required for their survival, Cell, 137(5): 873-886, 2009.
In this paper, we identify DEPTOR as a new protein interacting with mTOR. DEPTOR negatively regulates the action of mTOR,
a protein playing key roles in many human diseases. We show that DEPTOR expression is low is most cancers. Surprisingly,
DEPTOR is highly expressed in a subset of multiple myelomas (MM). We show that MM use DEPTOR to promote cell survival and
we show that the reduction in DEPTOR expression causes the death of these cancer cells. These results generate hope for
the treatment of MM.
3) Caron A, Baraboi ED, Laplante M*, Richard D* (*corresponding authors), DEP-domain
containing mTOR-interacting protein in the rat brain: distribution of expression and potential implication.
J Comp Neurol, epub, 2014.
In this study, we mapped the expression of DEPTOR in the rat brain and observed that it is expressed in regions of the
brain involved in the control of energy balance. We also show that DEPTOR expression is elevated in the hypothalamus of
obese animals, suggesting that DEPTOR could represent a target to improve energy balance in obesity.
4) Laplante M and Sabatini DM, mTOR signaling in growth control and disease,
Cell, 13;149(2):274-93, 2012.
In this article, we reviewed the knowledge of the mTOR signaling pathway and discussed about its implications in human
diseases. This review covers various aspects of mTOR biology and rapidly became a reference.
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Study of the molecular mechanisms regulating adipogenesis. Obesity is defined as the
excessive accumulation of adipose tissue and is an important cause of death worldwide. The prevalence of obesity is
increasing in many countries and authorities view this condition as one of the most serious public health problems.
Although changes in lifestyle are responsible for the increase in incidence of obesity, heritability studies provide
evidence for a substantial genetic contribution to obesity risk. This indicates that humans are not equally susceptible
to weight gain and that interaction between genes and environment plays fundamental roles in obesity development. Because
diet and physical activity have shown limited long-term success in reducing obesity, the improvement of our understanding
of the molecular mechanisms regulating food consumption and energy storage could help the development of new tools to
treat obesity and its related diseases.
Study of the mechanisms linking obesity to its metabolic complications. Obesity caused
by the imbalance of the energy balance severely impairs normal liver metabolism. Ectopic fat accumulation and chronic
inflammation observed in obese represent some factors contributing to the deterioration of glucose metabolism and lipid in
this tissue. Although our understanding of the mechanisms involved in the development of metabolic diseases associated
with obesity has greatly improved in recent decades, important questions are still without answer. For example, how the
liver communicates his physical and metabolic state to other tissues is still not well understood. In recent years, we
have observed that a protein called DEPTOR could play roles in the control of hepatic metabolism in response to nutritional
changes. With the use of transgenic mouse models allowing the deletion or the overexpression of DEPTOR, we try to
understand the role of this specific protein in hepatic metabolism, and its implication in the regulation of liver function
Study of the implication of MTOR signaling in health and diseases. The mechanistic
target of rapamycin (mTOR) is a kinase that plays a crucial role in controlling cell growth and metabolism. mTOR is found
in two complexes called mTOR complex 1 and 2 (mTORC1 and mTORC2). In response to nutrients and growth factors, these
complexes activate several anabolic processes including the synthesis of proteins and lipids. Studies indicate that these
complexes are highly active in many cancers and in obesity. In recent years, research groups have observed that in addition
to controlling protein synthesis, mTOR pathway profoundly affects gene transcription by directly modulating the activity
of several transcription factors. The objective of our work is to identify new transcription factors whose activity is
modulated by mTOR, to define the transcriptional signature of that association and to determine the implication of these
discoveries in health and diseases.