James J. Collins, Ph.D.

photo of Dr. James J. Collins

Professor, Biomedical Engineering
University Professor
The Collins Lab
Center for BioDynamics
Wyss Institute, Harvard University
Ph.D., Medical Engineering, University of Oxford
A.B., Physics, College of the Holy Cross
Email: jcollins@bu.edu
Phone: (617) 353-0390
Office: ERB 307

Research Interests

Synthetic biology; systems biology; noise-enhanced sensorimotor function.

Current Research

Dr. Collins’ research focuses on developing nonlinear dynamical techniques and devices to characterize, improve and mimic biological function. His specific interests include: (1) modeling, designing and constructing synthetic gene networks; (2) reverse engineering naturally occurring gene regulatory networks; and (3) developing noise-based sensory prosthetics.

Selected Recent Publications

Allison K, Brynildsen M, Collins JJ Metabolite-enabled Eradication of Bacterial Persisters by AminoglycosidesNature. 473: 216-220. (12 May 2011)

Lee H, Molla M, Cantor C, Collins JJBacterial Charity Work Leads to Population-Wide ResistanceNature. 467: 82-86 (2010)

Kohanski M, DePristo M, Collins JJSublethal Antibiotic Treatment Leads to Multidrug Resistance via Radical-Induced MutagenesisMolecular Cell. 37: 311-320 (2010)

Friedland A, Lu T, Wang X, Shi D, Church G, Collins JJSynthetic Gene Networks That CountScience. 324: 1199-1202 (2009)

Ellis T, Wang X, Collins JJDiversity-based, Model-guided Construction of Synthetic Gene Networks with Predicted FunctionsNature Biotechnology. 27 (5): 465-471 (2009)

Dwyer D, Kohanski M, Collins JJNetworking Opportunities for BacteriaCell. 135: 1153-1156 (2008)

Kohanski M, Dwyer D, Wierzbowski J, Cottarel G, Collins JJMistranslation of Membrane Proteins and Two-Component System Activation Trigger Antibiotic-Mediated Cell DeathCell. 135: 679-690 (2008)

Kohanski MA, Dwyer DJ, Hayete B, Lawrence CA and Collins JJA Common Mechanism of Cellular Death Induced by Bactericidal AntibioticsCell. 130: 797-810 (2007)

Deans TL, Cantor CR and Collins JJA Tunable Genetic Switch Based on RNAi and Repressor Proteins for Regulating Gene Expression in Mammalian CellsCell. 130: 363-372 (2007)

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