Our primary goal is to understand how signals and molecules are transmitted between the nucleus and cytoplasm across the nuclear envelope. We work to decipher the mechanism and structure of the machinery that executes these cellular processes.
In the Lamason lab, we investigate how intracellular bacterial pathogens hijack host cell processes to promote infection. In particular, we study how Rickettsia parkeri and Listeria monocytogenes move through our tissues via a process called cell-to-cell spread. We utilize cellular, molecular, genetic, biochemical and biophysical approaches to elucidate the mechanisms of spread in order to reveal key aspects of pathogenesis and host cell biology.
The Davis lab is working to uncover how cells construct and degrade complex molecular machines rapidly and efficiently. We apply a variety of biochemical, biophysical, and structural approaches including quantitative mass spectrometry and single particle cryo-electron microscopy to understand the detailed molecular mechanisms of these processes. Ongoing projects in the lab are focused on autophagy, an essential eukaryotic protein and organelle degradation pathway, and assembly of the ribosome, which is essential in all cells.
Our goal is to understand the ecology and evolution of ocean microbes and how they influence global biogeochemical cycles. We focus on the cyanobacterium Prochlorococcus, which is the smallest and most abundant microbe in ocean ecosystems — sometimes accounting for half the total photosynthetic biomass. We use this model system to study life across all scales — from the genome to the ecosystem.
We focus on the molecular entities controlling and coordinating RNA metabolism — that is, the compendium of processes that involve RNA, including protein synthesis, processing, modifications, export, translation and degradation. Our goal is to understand how different aspects of RNA metabolism are controlled to generate structure and function during development, as well as how mutations in components of the RNA metabolic program lead to congenital disorders and cancer.
We aim to understand the code for RNA splicing: how the precise locations of introns and splice sites are identified in primary transcripts and how its specificity changes in different cell types. Toward this end, we are mapping the RNA-binding affinity spectra of dozens of human RNA-binding proteins and integrating this information with in vivo binding and activity data. We are also studying the functions of 3’ untranslated regions, including their roles in mRNA localization and microRNA regulation. The lab uses a combination of computational and experimental approaches to address these questions.
We focus on the events that occur at the starting points of chromosome duplication. These DNA sequences — called “origins of replication” — are found at multiple sites on each eukaryotic chromosome and direct the assembly of replisomes, which replicate the DNA on both sides of the origin. We study this assembly process to understand how chromosomes are replicated, and how these events are regulated during the cell cycle to ensure genome maintenance.
We study microRNAs and other small RNAs that specify the destruction and/or translational repression of mRNAs. We also study mRNAs, focusing on their untranslated regions and poly(A) tails, and how these regions recruit and mediate regulatory phenomena.
We use genetic approaches to identify the molecular basis of human disease pathology. More specifically, we develop strategies to combat three major disease areas: cancer, trinucleotide repeat disorders like Huntington’s disease, and cardiovascular disease.
We combine comprehensive bioinformatics analyses with functional analyses of pathways and genes to study aging in humans and mice. We apply these approaches to identify the major pathways and genes involved in the aging of certain brain regions. We are also studying muscular dystrophy and muscle loss with aging. Ultimately, our findings may guide studies in other organs and lead to a systemic understanding of mammalian aging.