Jesse Rinehart

This study identifies and corrects fitness defects in genomically recoded E. coli, improving growth and functional capabilities.

The paper systematically optimizes an orthogonal translation system to enhance its biological tolerance by minimizing host interactions and stress responses.

The paper develops a platform to profile interactions between intracellular pathogens and the human phosphoproteome, identifying host-pathogen interactomes and expanding knowledge of viral protein function.

The paper shows hyperosmotic stress causes transcriptional repression but still leads to downstream-of-gene (DoG) transcripts, with Pol II interactome changes and Integrator complex disruption involved.