Thomas received his PhD in Microbiology at the University of Gothenburg in 1989 under the supervision of Staffan Kjelleberg working on the topic of how bacteria survive a conditionally induced, growth-arrested, G0–like state.  He continued studying this topic under the mentorship of Frederick C. Neidhardt at the University of Michigan, as a postdoctoral fellow. With Fred, he discovered, cloned, and characterized the gene/protein called the Universal Stress Protein A (UspA). Upon returning to Sweden, as an Assistant Professor at Lund University, he demonstrated that the global re-routing of the transcriptional apparatus during cellular growth arrest was governed by a trade-off mechanism, now called sigma factor competition. His work on a bacterial G0-like state also lead to the discovery that aberrant and slightly misfolded proteins are more susceptible to attack by reactive oxygen species, which pinpointed an up-till-then unknown pathway for protein oxidation and established E. coli as a model system for studying the mechanisms underlying oxidative attack to proteins in the context of chronological cellular aging. Upon expanding the studies of protein oxidation to other model systems, the laboratory discovered that oxidatively damage proteins are inherited in a asymmetrical fashion in S. cerevisiae - Specifically, damaged proteins are retained in old mother cells during cytokinesis allowing proteomic age characteristics to be reset in the cellular progeny. Thomas is a Member of the Royal Swedish Academy of Sciences, Class VI, the American Academy of Microbiology, the American Society for Biochemistry and Molecular Biology, and EMBO.