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Home > Research > Faculty Research Interests > Michael Shapira
Michael Shapira
Assistant Adjunct Professor
Lab: Shapira Lab
Email: mshapira@berkeley.edu
Office phone: 643-2579
Research interests
The outcome of the interactions between a pathogen and its host is determined by the virulence factors employed by the pathogen, the immune system of the host and the ability of the two organisms to respond to attacks on their well-being or resources with counter-attacks. It is a dynamic process, which is additionally affected by environmental factors - the host is a niche for the pathogen, and both host and pathogen are affected by the niche inhabited by the host. Such ecological constraints shape the evolution of the two interacting organisms and in some cases lead to co-evolution. Understanding the interplay between host, pathogen and the environment over the time scale of the interactions, but also over an evolutionary time scale, is important for understanding infectious diseases.My research program seeks to understand the fundamentals of host-pathogen interactions in the context of the whole organism. We are interested in the mechanistic details of these interactions, but we are also considering the natural context in which these interactions have evolved and in which they occur. To this end, we are using the soil nematode Caenorhabditis elegans, a powerful model organism for genetic studies, as a host model. On the host side our goals are to understand how pathogens are recognized, how this recognition is translated into the appropriate response, what are the specific mechanisms that direct responses to biotic or abiotic stress conditions and what is their capacity to integrate such signals. As an extension of this, we are further focusing on the interface between infection and aging. On the pathogen side, our goals are to characterize natural interactions between C. elegans and the microbial world, focusing on the worm gut microflora, as well as to better understand the mechanisms underlying bacterial evolution and the consequences of evolution under stress conditions for pathogen virulence.
Current projects in the lab include: 1) Pathogen recognition and response initiation 2) MAPK signaling in biotic and abiotic stress responses 3) Infection and life history traits 4) Host pathogen interactions between C. elegans and the human food-borne pathogen Salmonella typhimurium. 5) C. elegans natural gut microflora 6) Evolution of Salmonella under conditions of ionizing radiation.
Students are encouraged to learn a wide array of methodologies and techniques, including worm genetics, microbiology, molecular biology, fluorescent microscopy, quantitative RT-PCR and microarray gene expression analyses, leading to independent research on any aspect relevant to environmental stress or host-pathogen interactions.
Selected publications
Shapira, M. and Tan, M-W. Genetic analysis of C. elegans innate immunity (2008) Methods Mol. Biol. 415, 429-42.Kurz, C.L., Shapira, M., Chen, K., Baillie, D.L. and Tan, M.W. (2007) C. elegans pgp-5 is involved in resistance to bacterial infection and heavy metal and its regulation requires TIR-1 and a p38 MAP kinase cascade. Biochem. Biophys. Res. Commun. 363(2): 438-43.
Shapira, M. Hamlin, B.J., Rong, J., Chen, K., Ronen, M. and Tan, M.W. (2006) A conserved role for a GATA transcription factor in regulating epithelial innate immune responses. Proc. Natl. Acad. Sci. USA 103: 14086-14091.
Shapira, M. Segal, E. and Botstein, D. (2004) Disruption of yeast forkhead-associated cell cycle transcription by oxidative stress. Mol. Biol. Cell. 15: 5659-5669.
Segal, E., Shapira, M., Regev, A., Pe’er, D., Botstein, D., Koller, D and Friedman, N. (2003) Module Networks: Discovering Regulatory Modules and their Condition Specific Regulators from Gene Expression Data. Nat. Genet 34(2): 166-176.


