Grand Prize Winner – Dr. Liron Bar-Peled
Lallage Feazel Wall Fellow of the Damon Runyon Cancer Research Foundation and Research Associate researcher at Scripps Research Institute in La Jolla, USA
From: Rehovot, Israel
Prize category: Cell and Developmental Biology
Essay: Size does matter
Dr. Bar-Peled received his Bachelor of Science degree in biochemistry from the University of Georgia and his PhD in biology from the Massachusetts Institute of Technology, where he studied amino acid sensing in David Sabatini’s lab
He is a recipient of the 2014 Weintraub Award for Graduate Research, the 2013 Gary Bokoch memorial award from the American Society for Biochemistry and Molecular Biology and the 2012 Abraham J. Siegel Fellowship Award from the Whitehead Institute for Biomedical Research. He is currently investigating how cells respond to oxidative stress in the laboratory of Professor Benjamin Cravatt at the Scripps Research Institute in La Jolla. He is a Lallage Feazel Wall Fellow of the Damon Runyon Cancer Research Foundation.
The enzyme mTORC1 functions as master regulator of eukaryotic cell growth and is deregulated in some common cancers and diabetes. It senses a diverse array of environmental stimuli, including amino acid levels, via a complex pathway that includes a family of molecular switches called Rags. The research described in this essay focused on understanding this pathway by identifying protein factors that form a lysosome-based signaling platform that positively and negatively regulates the function of the Rags. The essay also describes evidence indicating how dereg- ulation of this amino acid sensing pathway is related to human diseases.
Category winner – Dr. Dan Dominissini
Human Frontier Science Program (HFSP) postdoctoral fellow in the laboratory of Professor Chuan He at the University of Chicago, USA
From: Tel-Aviv, Israel
Prize Category: Genomics and Proteomics
Essay: Roadmap to the Epitranscriptome – N6-methyl-adenosine Signals the Way, YTH Proteins
Dr. Dominissini received his Bachelor of Medical Science degree from Tel-Aviv University, Israel, in 2007. He went on to study RNA post-transcriptional modifications for his PhD, focusing on adenosine deamination and methylation, with Gideon Rechavi at Tel-Aviv University. He is currently a Human Frontier Science Program (HFSP) postdoctoral fellow in the laboratory of Professor Chuan He at the University of Chicago, Illinois, USA, where he develops novel chemistries for the study of nucleic acid modifications.
An extensive repertoire of chemical modifications decorates RNA to expand its vocabulary, thereby helping it fulfill its roles in a variety of biological processes. One such prevalent and essential modification is methylation on the N6 position of adenosine. Dr. Dominissini developed a global RNA N6-methyladenosine (m6A) sequencing method to reveal principles that govern m6A distribution and function. Several of the major proteins binding to m6A were identified, and methylation was shown to be dynamically deposited on RNA, in a pattern that it is highly conserved during evolution.
Category winner – Dr. Chelsea Wood
Fellow in the Michigan Society of Fellows and an Assistant Professor in the Department of Ecology and Evolutionary Biology at the University of Michigan, USA
From: Long Island, USA
Prize Category: Environment
Essay: Environmental change and the ecology of infectious disease
Dr. Wood is a disease ecologist interested in how parasites and pathogens respond to human impacts on the environment. She received her Bachelor of Arts degree from Dartmouth College, and her PhD from Stanford University. She did postdoctoral research in Associate Professor Pieter Johnson’s lab at the University of Colorado at Boulder, and is currently a Fellow in the Michigan Society of Fellows and an Assistant Professor in the Department of Ecology and Evolutionary Biology at the University of Michigan.
Does loss of biodiversity generally increase or decrease disease agent transmission? In other words, do human impacts on biodiversity increase the prevalence of diseases by eroding natural “checks and balances” on transmission or decrease prevalence when they remove the free-living biodiversity on which disease agents depend? Dr. Wood approached this question using fished marine food webs as model systems. The research described in her essay suggests that the impacts of fishing on parasites are complex but predictable with an understanding of parasite natural history.
Category winner – Dr. Simon Johnson
American Federation for Aging Research Fellow at the Albert Einstein College of Medicine in New York; USA
From: Salt Lake City, USA
Prize Category: Translational Medicine
Essay: A Novel Target for Pharmacological Intervention in an Untreatable Human Disease
Dr. Johnson is an American Federation for Aging Research Fellow in the department of Genetics at the Albert Einstein College of Medicine in New York. He earned his Bachelor of Science degree in Biochemistry and Biophysics at Oregon State University and received his PhD from the University of Washington, Department of Pathology, in the Molecular Basis of Disease. He was a 2009 Howard Hughes Medical Institute EXROP scholar and was previously supported by the Nathan Shock Center Genetic Approaches to Aging pre-doctoral and Mechanisms of Cardiovascular Diseases post-doctoral competitive training grants. His current work is centered on characterizing the role of naturally occurring genetic variation in insulin/IGF-1/mTOR signaling genes on human longevity.
Mitochondrial dysfunction contributes to a variety of pathological conditions, and identifying treatment strategies is a major translational research goal. Severe defects in mitochondrial proteins are associated with fatal childhood diseases, including Leigh Syndrome. In a yeast genetic screen, mitochondrial mutants were highly enriched among strains that positively respond to caloric restriction. As a result of this finding, rapamycin (which inhibits the mTOR nutrient-signaling path- way) was tested in a mouse model of Leigh Syndrome. Rapamycin dramatically attenuated disease in these mice, and diseased mice showed increased signaling through mTOR in the absence of treatment.