Christine Jacobs

This paper develops antimicrobial polyacrylamides using a cross-molecular machine learning pipeline trained on antimicrobial peptides, showing synergy with clinical drugs against E. coli biofilms.

This study identifies HMGR as a critical enzyme in B. burgdorferi's mevalonate pathway, revealing its cofactor promiscuity and evolutionary significance.

This paper identifies BbbA and BbbB as essential bactofilins that organize peptidoglycan insertion sites in Borrelia burgdorferi, critical for cell growth and viability.

This study identifies a complex lipid profile in Borrelia burgdorferi, revealing its reliance on environmental lipids and its ability to synthesize eukaryotic-like lipids.

The paper investigates priority effects between fungi and nematodes in insect larvae, finding that fungi arrive first and exclude nematodes, with a bacterium mediating this exclusion.

The paper shows glycogen phase separation in E. coli causes asymmetric division and macromolecular rearrangement during growth phase transition.

This study identifies PAPI (encoded by pcnB) as essential for maintaining virulence and AMR plasmid copy number, stability, and bacterial virulence in Yersinia and Shigella.

The paper develops a time-resolved single-cell pipeline to analyze antimicrobial peptides in E. coli, revealing two classes with opposing functional trade-offs in their mechanisms and efficacy against biofilms.

The paper identifies ruptoblasts, a novel cytotoxic cell type in planarians, showing they use explosive cell death to release cytotoxic agents in response to activin, linking hormonal regulation to immune defense.

This paper shows that Borrelia burgdorferi loses genetic elements and proliferative ability in lab cultures during starvation but maintains these traits in tick vectors.

This study identifies bacterial enzymes that modify peptidoglycan fragments from Borrelia burgdorferi, showing they are poor immune stimulators and that host enzymes like PGLYRP2 are less active in joint fluids, contributing to persistent arthritis.

The paper shows genome concentration limits transcription and affects proteome composition in E. coli, with effects detectable in nutrient-rich conditions.

The paper shows that polysome dynamics in E. coli help segregate chromosomes during cell division, linking this process to cell growth.

This study shows that Caulobacter crescentus daughter cells have different growth rates due to a G1 phase slowdown, mediated by (p)ppGpp, linking growth modulation to asymmetric division and cell cycle regulation.

This study characterizes the organization of Borrelia burgdorferi's segmented genome and interactions between replicons using Hi-C, revealing chromosome structure and plasmid interactions.

The paper quantifies cell cycle phenotypes in E. coli and identifies robust rules linking cell size to division processes across nutrient conditions.

The paper develops a theoretical framework to explain exponential growth in nonlinear reaction networks, showing how scalability of flux functions and ergodicity of rescaled systems lead to various growth modalities.

The paper shows that RNA polymerases in E. coli exhibit collaborative and antagonistic behaviors due to DNA supercoiling during transcription.

The paper develops a stochastic model of bacterial gene expression to show how mRNA degradation and transcriptional pausing influence protein expression noise.