Program Faculty

 The long-term goal of my research program is to understand at atomic resolution the mechanistic underpinnings of stress responses. These are essential for survival in all organisms, and often rely on the interplay between cellular pathways used to control genome integrity and transcriptional programs. My interests stem from my previous studies of transcription and DNA repair ATPases. As such, my lab’s work has centered on the regulation of RpoS, the master regulator of the general stress response in g-proteobacteria, and Mfd, a widely conserved bacterial transcription-repair coupling factor involved in the response to DNA damage. Our current goal is to decipher, structurally and functionally, how these key factors regulate transcription, promote the preferential repair of active genes, mediate hypermutation and the acquisition of antibiotic resistance. In the last ten years, my group’s contributions have facilitated the understanding of the macromolecular interactions that are being sculpted during stress responses and lead to accelerated molecular evolution and underly both genomic integrity and genetic diversity. This work has direct relevance for antibiotic development via anti-evolution drugs and the dissection of cellular mechanisms involved in bacterial virulence and the generation of genetic diversity.

Publications