Nick Davis (DEDON LAB)

Epitranscriptomics: A System of tRNA Modifications Control Mycobacterial Drug Resistance

My research aims to advance our fundamental understanding of how translation regulates cell phenotype. I am developing a translational model for how Mycobacterium tuberculosis, the world’s more pervasive pathogen, survives the stress of infection. Integrating in-house methods to study post-transcriptional biology with quantitative proteomics and whole-genome codon usage analysis, I have identified tRNA modification enzymes as potential antibiotic targets. Ultimately, my work looks to establish a general approach for anti-infectives discovery.

Galit Frydman (FOX LAB)

The Megakaryocyte: A New Innate Immune Cell and Its Potential Role in Sepsis

Sepsis is a leading cause of death in intensive care units, with a mortality rate between 30-40%. Platelets, the progeny of megakaryocytes, have been demonstrated to play a key role in immune-thrombosis during critical illness. Changes in platelets have been proposed to be secondary to alterations in megakaryo- and thrombopoiesis. We hypothesize that sepsis results in aberrant megakaryopoiesis, resulting in a pro-inflammatory megakaryocyte and platelet phenotype, exacerbating the pathophysiology of this disease.