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A novel dual genome approach that combines genetically diverse mice and a library of bacterial mutants to define the genome-wide host pathogen interactions that drive distinct outcomes to tuberculosis.

Point mutations in a ubiquitous human ATPase called p97/VCP deregulate inter-domain communication, resulting in impaired binding of an adaptor that recruits p97 to endosomal pathways and leading to a degenerative disease of bone, muscle and neurons.

The ability of the T cell receptor to discriminate ligands is imperfect, allowing T cells to respond to ultra-low-affinity ligands.

Prokaryotic TRADD-N and Death-like adaptor domains in diverse predicted apoptosis and immune systems from multicellular prokaryotes and metazoans indicate the common origin of key apoptosis mechanisms required for the stabilization of multicellularity.