Conversion of Escherichia coli to Generate All Biomass Carbon from CO.

The living world is largely divided into autotrophs that convert CO into biomass and heterotrophs that consume organic compounds. In spite of widespread interest in renewable energy storage and more sustainable food production, the engineering of industrially relevant heterotrophic model organisms to use CO as their sole carbon source has so far remained an outstanding challenge. Here, we report the achievement of this transformation on laboratory timescales.

The genetic basis for the adaptation of E. coli to sugar synthesis from CO.

Understanding the evolution of a new metabolic capability in full mechanistic detail is challenging, as causative mutations may be masked by non-essential "hitchhiking" mutations accumulated during the evolutionary trajectory. We have previously used adaptive laboratory evolution of a rationally engineered ancestor to generate an Escherichia coli strain able to utilize CO fixation for sugar synthesis. Here, we reveal the genetic basis underlying this metabolic transition.

Sugar Synthesis from CO2 in Escherichia coli.

Can a heterotrophic organism be evolved to synthesize biomass from CO2 directly? So far, non-native carbon fixation in which biomass precursors are synthesized solely from CO2 has remained an elusive grand challenge. Here, we demonstrate how a combination of rational metabolic rewiring, recombinant expression, and laboratory evolution has led to the biosynthesis of sugars and other major biomass constituents by a fully functional Calvin-Benson-Bassham (CBB) cycle in E. coli.

Acetohydroxyacid synthase from Mycobacterium avium and its inhibition by sulfonylureas and imidazolinones.

Tuberculosis (TB) remains one of the world's leading causes of death from infectious disease. It is caused by infection with Mycobacterium tuberculosis or sometimes, particularly in immune-compromised patients, Mycobacterium avium. The aim of this study was to create a tool that could be used in the search for new anti-TB drugs that inhibit branched-chain amino acid (BCAA) biosynthesis, as these are essential amino acids that are not available to a mycobacterium during growth in an infected organism.