Pere Puigserver, PhD
Office phone: 617-582-7977
Website: Puigserver Lab
Preferred contact method: email
Area of Research
Nutrient Sensing, Mitochondrial Biology and Cancer Metabolism
Dana-Farber Cancer Institute
450 Brookline Avenue
Boston, MA 02215
Pere Puigserver is a Professor of Cell Biology at Harvard Medical School. His laboratory is based in the Department of Cancer Biology at Dana-Farber Cancer Institute, located in the Center for Life Sciences Boston (CLSB).
Dr. Puigserver received his B.S. in Biological Sciences and Ph.D. in Biochemistry at the University of Illes Balears, Spain. His graduate work focused on mitochondrial energetics using in-vitro and in-vivo approaches, and included research at the University of Stockholm. He pursued postdoctoral training in molecular and cellular biology at the Dana-Farber Cancer Institute and Harvard Medical School. In 2002, he was appointed Assistant Professor of Cell Biology at Johns Hopkins University School of Medicine. In 2006, he was recruited back to the Dana-Farber Cancer Institute and Harvard Medical School to continue his research program in cell metabolism.
ResearchNutrient Sensing, Mitochondrial Biology and Cancer Metabolism
The Puigserver Laboratory investigates broad aspects of fundamental metabolic and energetic processes in mammals that are necessary for cell survival and specific biological function. We focus on the molecular mechanisms by which mammalian cells sense, communicate, and respond to nutrients.
Studies from our group have identified new basic and evolutionary conserved metabolic circuitries that involve nutrient signaling to gene expression programs associated with cellular metabolic reprogramming. Components of these circuitries are dysregulated in metabolic diseases, cancer, and age-associated diseases and represent therapeutic targets.
The Lab’s research program pursues fundamental biological and disease-relevant questions such as:
- What are the molecular components that sense and transmit nutrient signals to reprogram mammalian cells?
- What are the molecular components that sense signals to coordinate the supply of proteins for mitochondrial biogenesis, dynamics, and function?
- What are the genetic and epigenetic mechanisms underlying metabolic reprogramming and plasticity in tumor cells?
The Puigserver Lab’s research combines and applies a variety of biochemical, cellular, genetic, chemical biology, metabolic, and screening approaches both in cell culture and whole animals to identify the molecular mechanisms by which mammalian cells sense, communicate, and respond to nutrients. In particular, we have a close collaboration with the Broad Institute in chemical biology to identify small compounds involved in nutrient sensing and metabolic reprogramming in a variety of mammalian cell types.
- Rodgers JT, Lerin C, Haas W, Gygi SP, Spiegelman BM, Puigserver P. 2005. Nutrient control of glucose homeostasis through a complex of PGC-1alpha and SIRT1. Nature, 434, 113-8.
- Lerin C, Rodgers JT, Kalume DE, Kim SH, Pandey A, Puigserver P. 2006. GCN5 acetyltransferase complex controls glucose metabolism through transcriptional repression of PGC-1alpha. Cell Metab, 3, 429-38.
- Cunningham JT, Rodgers JT, Arlow DH, Vazquez F, Mootha VK, Puigserver P. 2007. mTOR controls mitochondrial oxidative function through a YY1-PGC-1alpha transcriptional complex. Nature, 450, 736-40.
- Gerhart-hines Z, Rodgers JT, Bare O, Lerin C, Kim SH, Mostoslavsky R, Alt FW, Wu Z, Puigserver P. 2007. Metabolic control of muscle mitochondrial function and fatty acid oxidation through SIRT1/PGC-1alpha. EMBO J, 26, 1913-23.
- Schafer ZT, Grassian AR, Song L, Jiang Z, Gerhart-Hines Z, Irie HY, Gao S, Puigserver P, Brugge JS. 2009. Antioxidant and oncogene rescue of metabolic defects caused by loss of matrix attachment. Nature, 461, 109-13.
- Dominy JE, Gerhart-Hines Z, Puigserver P. 2011. Nutrient-dependent acetylation controls basic regulatory metabolic switches and cellular reprogramming. Cold Spring Harb Symp Quant Biol, 76, 203-9.
- Gerhart-Hines Z, Dominy JE, JR, Blattler SM, Jedrychowski MP, Banks AS, Lim JH, Chim H, Gygi SP, Puigserver P. 2011. The cAMP/PKA pathway rapidly activates SIRT1 to promote fatty acid oxidation independently of changes in NAD(+). Mol Cell, 44, 851-63.
- Dominy JE, Jr, Lee Y, Jedrychowski MP, Chim H, Jurczak MJ, Camporez JP, Ruan HB, Feldman J, Pierce K, Mostoslavsky R, Denu JM, Clish CB, Yang X, Shulman GI, Gygi SP, Puigserver P. 2012. The deacetylase Sirt6 activates the acetyltransferase GCN5 and suppresses hepatic gluconeogenesis. Mol Cell, 48, 900-13.
- Blattler SM, Cunningham JT, Verdeguer F, Chim H, Haas W, Liu H, Romanino K, Ruegg MA, Gygi SP, Shi Y, Puigserver P. 2012. Yin Yang 1 deficiency in skeletal muscle protects against rapamycin-induced diabetic-like symptoms through activation of insulin/IGF signaling. Cell Metab, 15, 505-17.
- Blattler SM, Verdeguer F, Liesa M, Cunningham JT, Vogel RO, Chim H, LiuH, Romanino K, Shirihai OS, Vazquez F, Ruegg MA, Shi Y, Puigserver P. 2012. Defective mitochondrial morphology and bioenergetic function in mice lacking the transcription factor Yin Yang 1 in skeletal muscle. Mol Cell Biol, 32, 3333-46.
- Vazquez F, Lim JH, Chim H, Bhalla K, Girnun G, Pierce K, Clish CB, Granter SR, Widlund HR, Spiegelman BM, Puigserver P. 2013. PGC1alpha expression defines a subset of human melanoma tumors with increased mitochondrial capacity and resistance to oxidative stress. Cancer Cell, 23, 287-301.
- Dominy, John, PhD
- Lim, Ji-Hong, PhD
- Sharabi, Kfir, PhD
- Rines, Amy, PhD
- Tabata, Mitsuhisa, MD, PhD
- Chi, Lou, PhD
- Hall, Jessica, Graduate Student
- Lee, Yoonjin, Graduate Student