Tom Maniatis, PhD
Dr. Maniatis is known for pioneering the development of gene cloning technology and its application to both basic research and biotechnology. He also coauthored the definitive laboratory manual on Molecular Cloning. His research has led to fundamental advances in understanding the mechanisms of gene regulation and RNA splicing, the biochemistry of innate immunity signaling pathways, the function of single cell diversity in the nervous system, and neurodegenerative disease mechanisms. Dr. Maniatis received his B.A. and MS. degrees from the University of Colorado in chemistry and biology, and his Ph.D. in molecular biology from Vanderbilt University. After postdoctoral studies at Harvard University and the Laboratory of Molecular Biology, Cambridge, England, Dr. Maniatis was a professor at the California Institute of Technology and subsequently at Harvard University.
- Isidore S. Edelman Professor of Biochemistry and Molecular Biophysics
- Director, Columbia University Precision Medicine Initiative
- Executive Committee, Zukerman Mind Brain Behavior Institute
- Principal Investigator, Maniatis Lab
- Scientific Director and Chief Executive Officer of the New York Genome Center
Credentials & Experience
Education & Training
- BA, 1965 Biology, University of Colorado
- MS, 1967 Chemistry, University of Colorado
- PhD, 1971 Molecular Biology, Vanderbilt University
Honors & Awards
Dr. Maniatis’ research has been recognized by many awards, including the Eli Lilly Award in Microbiology and Immunology, The Richard Lounsbery Award for Biology and Medicine (Awarded by the French and U.S National Academy of Sciences), and the 2012 Lasker-Koshland Special Achievement Award in Medical Science. He is a member of the U.S. National Academy of Science, the U.S. Academy of Medicine, and a fellow of the U.S. Academy of Arts and Sciences.
The primary focus of my lab during the past 10 years has been in two areas: 1. Disease mechanisms of ALS, which involves a combination of human genetic, stem cell and animal model approaches, and 2. The structure and function of the clustered protocadherin (Pcdh) genes. We have used behavioral assays in both projects to characterize the phenotypic consequences of mutations in mouse models. The ALS animal model work has involved the use of various neuromuscular behavioral studies of the SOD1 G93A mouse model, while the protocadherin project has involved studies of both motor function and affective behavior (depression and anxiety). Manuscripts describing both studies are under review. The most recent ALS work is a study of the role of autophagy in ALS disease progression, and these studies involved various studies of motor function such as the rotarod test for motor coordination and muscle strength. The protocadherin studies involve various assays for affective function (anxiety and depression), in Pcdha gene cluster deletion mice. We have shown that these mice display a cell-autonomous serotonergic wiring phenotype, and have characterized the behavioral consequences. Recent human genetic studies from other laboratories have implicated the Pcdh gene cluster in autism and other neurological diseases. We have generated a series of well-characterized deletion mutants in the Pcdh gene cluster, and are characterizing their behavioral phenotypes. Thus, the behavior core is central to our ongoing and future studies.
- ALS Disease Mechanisms
- Genetic Basis of Neurological Diseases
- Neurobiology of Disease
- Regulation of RNA Transcription and Splicing
- Stem Cell Biology
- Synapses and Circuits
- The Role of Neuroinflammation in ALS