My research has primarily focused on persister formation in Escherichia coli. The goal of my research is to understand the genetic basis of persister formation using Escherichia coli as a model. In collaboration with Dr. Andy Camilli lab at Tufts University, I apply transposon sequencing (Tn-seq) to quantify role of each gene on persister formation in vitro as well as during treatment of an infectious model. Together with Sarah Rowe, a former postdoc, we developed a cell sorting based method to evaluate persister levels in different fractions of a given population. I seek to answer the questions including what molecular pathways lead to antibiotic tolerance, how environmental signal affects persister level and how each reported mechanism contribute to persister formation during infection. Answering these questions will lead to the discovery of novel antibiotic that can eliminate persisters and sterilize infections.
Publication since joining Lewis lab:
Lewis K, Shan Y. 2017. Why tolerance invites resistance. Science 355 (6327):796
Shan Y*, Brown Gandt A*, Rowe SE,Deisinger JP, Conlon BP, Lewis K. 2017. ATP dependent persister formation in Escherichia coli. mBio 8:e02267-16.*equal contribution
Jones MB, Nierman WC, Shan Y, Frank BC, Spoering A, Ling L, Peoples A, Zullo A, Lewis K, Nelson KE. 2016 Reducing the Bottleneck in Discovery of Novel Antibiotics. Microb. Ecol.
Lewis K, Shan Y. 2016. Persisters awakening. Mol. Cell. 63(1):3-4
Shan Y, Lazinski D, Rowe S, Camilli A, Lewis K. 2015. Genetic basis of persister tolerance to aminoglycosides in Escherichia coli. mBio 6(2):e00078-15