Dr. Michael Lawson obtained his B.A. in Chemistry from Pomona College, where he studied the regiospecificity of metalloenzymes with Professor Matthew Sazinsky. He then spent a year as a Fulbright Scholar in Professor Wolfgang Sippl’s lab at Martin Luther Universität in Germany, using computational techniques to search for selective inhibitors of histone deacetylases. As an NSF Graduate Fellow with Professor James Berger at UC Berkeley, he employed structural and biochemical techniques to determine how the bacterial transcription termination factor Rho is controlled by nucleic acids, small molecules, and dissociable protein cofactors. As an A.P. Giannini and K99/R00 Postdoctoral Fellow with Professor Joseph Puglisi at Stanford, he used an in vitro-reconstituted translation system and single-molecule assays to uncover the basis of speed and fidelity in eukaryotic translation termination. Mike joined the UCLA faculty in 2023. His laboratory uses biochemical, biophysical, and structural techniques to examine mechanisms of eukaryotic translational quality control.
Significant differences are observed when normal or aberrant mRNAs are translated by ribosomes. Normal mRNAs are typically released and can be translated again, while problematic mRNAs are recognized and targeted for decay. However, the molecular events that underlie these decisions are not well understood. Since issues with translation can cause many diseases, better understanding of these mechanisms could help develop treatments for conditions such as cystic fibrosis, muscular dystrophy, and cancer.
The Lawson lab aims to understand how ribosomes, mRNA sequence and structure, and specialized decay factors work together to differentiate normal from problematic mRNAs. These interactions are challenging to study using conventional methods due to their dynamic and transient nature. Therefore, we employ biochemical, biophysical, and structural methods, as well as in vitro-reconstituted translation systems, to investigate how normal and problematic mRNAs are translated differently and how decay factors detect defects. Ultimately, this understanding may lead to new treatments for the ~11% of heritable human diseases caused by premature stop codons.
Honors & Awards
- NIH K99/R00 Pathway to Independence Award, 2022
- A.P. Giannini Foundation Postdoctoral Fellowship, 2018
- Outstanding Graduate Student Instructor Award, UC Berkeley, 2012
- NSF Graduate Research Fellowship, 2011
- Fulbright Research Scholar, 2009