In our laboratory, we take an interdisciplinary approach to study the fundamental mechanisms by which bacteria grow, divide, and adapt to changing growth conditions. We use the dimorphic α-proteobacterium Caulobacter crescentus as our primary model for these studies, as its curved-rod morphology and well-characterized cell and developmental cycle make it particularly well-suited to address questions of morphogenesis and growth control. To do this, we use a multi-pronged approach combining genetics, genomics, imaging, biochemistry, and in vitro reconstitution to get to molecular mechanisms. We are highly collaborative and love to work with specialists in advanced imaging techniques, new analytical approaches and tools, structural biology, and complementary model organisms. Our fundamental research into essential aspects of bacterial physiology will inform antibiotic development and resistance mechanisms, as well as synthetic cell biology efforts. Currently we are investigating molecular mechanisms by which bacterial growth is regulated at both a global and a local level.

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Current Questions:
How is bacterial growth regulated locally during cell division?
The polymerizing GTPase FtsZ is a master regulator of bacterial cell division. Recent work from our lab and others suggests that FtsZ is a “dynamic activator” of the peptidoglycan cell wall synthesis that drives division. We are asking the following questions to address this model:
How does the structure and dynamics of the polymerizing GTPase FtsZ impact its function, and how are these regulated?
What are the physical and functional links between the FtsZ cytoskeleton and peptidoglycan metabolic enzymes?
How are the late stages of cell division mediated?
How is cell division coordinated with other morphogenetic events?

How is bacterial growth and morphogenesis regulated globally under changing environmental conditions?
As single-celled organisms, bacteria can experience rapid changes in environmental conditions, including the availability of nutrients. Cell cycle progression, cell shape, and growth are altered to promote survival when cells experience nutrient limitation through mechanisms that are not entirely clear. We are asking:
How is the transcriptome reprogrammed during starvation to promote survival?
How are cell biological processes, specifically cell cycle progression and morphogenesis, differentially regulated during activation of the stringent response?
How do alterations to metabolic flux impact cell morphology and cell cycle progression?