Colleagues: Recently Tenured


Michael Grigg

Senior Investigator; Chief, Molecular Parasitology Unit, Laboratory of Parasitic Diseases

Education: University of British Columbia, Vancouver, Canada (B.Sc. in biochemistry); Imperial College of Science, Technology, and Medicine, University of London, London (Ph.D. in biochemistry; D.I.C.)
Training: Howard Hughes Medical Institute senior fellow at the University of Washington (Seattle); postdoctoral scholar in molecular parasitology at Stanford University (Stanford, Calif.)
Before coming to NIH: Assistant professor of medicine, microbiology, and immunology at the University of British Columbia
Came to NIH: In 2006 as a tenure-track investigator in NIAID’s Laboratory of Parasitic Diseases
Selected professional activities: Fellow of the Canadian Institute for Advanced Research’s Integrated Microbial Biodiversity Program
Outside interests: Running marathons; rowing; kayaking; spending time in the outdoors

Research interests: The Molecular Parasitology Unit uses population-, forward-, and reverse-genetics techniques to understand the molecular basis of virulence and pathogenesis in parasitic protozoa. Protozoal zoonoses (diseases that can be naturally transmitted from animals to humans) are serious pathogens of humans and animals throughout the world. By studying these protozoa, scientists have gained significant insights into fundamental processes such as antigenic variation, virulence shifts, and RNA editing.

My program’s focus is on the food- and water-borne parasite Toxoplasma gondii, a pathogen that causes lethal infections in developing fetuses and immunocompromised patients. It also causes blinding chorioretinitis, an inflammation of the retina, in children and adults. In all hosts, T. gondii establishes life-long infections. Despite its prevalence as a human pathogen, surprisingly little is known about how it causes disease. What’s more, there is no vaccine or drug that can control it.

Our laboratory has developed new genetic, genomic, and molecular-imaging techniques to identify—in animal models of infection—the genes that enable these parasites to enter and colonize host cells, evade the immune system, and cause virulent disease. Virulence is a critical pathogen-enhancing determinant of infectious diseases. Our studies are establishing how virulence emerges, how it is propagated by parasite sexual cycles, and how it is maintained in complex genetic populations circulating in the vast array of intermediate hosts these parasites infect. Our work deals with the genetic origins of outbreaks caused by a large and diverse group of eukaryotic pathogens, including species of Toxoplasma, Plasmodium (the causative agent of malaria), Cryptosporidium, Leishmania, and Giardia.

Because little is known about eukaryotic pathogenic processes compared with those of bacterial or viral pathogenesis, entirely new mechanisms and principles of pathogenesis are emerging from our work


Sushil Rane

Senior Investigator; Chief, Cell Growth and Metabolism Section

Education: University of Bombay, Mumbai, India (B.S. and M.S. in biology and biochemistry); Temple University, School of Medicine, Philadelphia (Ph.D. in biochemistry)
Training: Postdoctoral fellowships at Bristol-Myers Squibb Pharmaceutical Research Institute (Princeton, N.J.) and at Fels Research Institute (Philadelphia)
Came to NIH: In 2001 as NCI Scholar; in 2006 became tenure-track investigator in NIDDK
Selected professional activities: Reviewing manuscripts; organized a TGF-beta Special Interest Group on campus
Outside interests: Coaching baseball teams that his two sons play on

Research interests: My research group studies the molecular underpinnings of glucose and energy balance to better understand obesity and diabetes. We focus on the cell cycle—how cells divide and replicate. Using mouse models, we study how the cell cycle influences glucose regulation, energy homeostasis, and beta cells.

Beta cells store and release insulin and are found in the pancreas. My group showed that a key cell-cycle protein, Cdk4, regulates beta-cell mass, a finding that may have potential clinical applications for diabetes therapy. Currently, we are investigating molecular pathways involving cell-cycle regulators that lead to increases in beta-cell mass and improvements in beta-cell function.

We also study how cell-cycle proteins influence the growth, development, differentiation, and death of cells that comprise the organs that maintain normal glucose tolerance and glucose homeostasis. Our goal is to determine how the expression of cell-cycle molecules and their resultant biological pathways differ in obesity and diabetes.

We demonstrated that the TGF-beta signaling pathway regulates glucose tolerance and energy homeostasis and that it controls the acquisition of properties of metabolically beneficial brown fat within the often problematic white fat. The switch of white fat to brown fat may protect against obesity and diabetes. We strive to further characterize the mechanisms involved in the switch.

We hope our findings will provide an integrated view into multiorgan communication as it relates to glucose homeostasis and energy balance. Ideally, this information will deepen our understanding of the pathogenesis of diabetes and obesity, leading to the development of rational therapies.