Selective constraints on bacterial signaling proteins

2 Dec 2011

Michael Laub
Department of Biology, MIT


Our lab is interested in the specificity and evolution of signaling pathways. We study two-component signal transduction systems, the predominant form of signaling in bacteria, which involve sensor histidine kinases and their cognate substrates. We have previously shown that the specificity of kinase-substrate interactions is dictated at the level of molecular recognition and relies on a relatively small set of residues. We can now probe the evolution of kinase-substrate specificity by focusing on changes that occur to these residues. We are probing the selective pressures that influence these residues and, in particular, trying to understand how gene duplication impacts specificity. For example, how are the proteins produced by duplication insulated from one another and from other existing pathways? Can we infer the mutational trajectories followed by duplicates and what, if anything, constrains these trajectories?

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