Dr. Kanchan Jaswal recently completed her Ph.D. under the mentorship of Dr. Rachna Chaba at the Indian Institute of Science Education and Research (IISER) Mohali. Her doctoral research explored the interplay between carbon metabolism, the electron transport chain, and envelope redox homeostasis in Escherichia coli. Looking ahead, she aspires to investigate key questions in host–gut microbiome interactions.
As part of her Ph.D., she published a paper titled “Metabolism of long-chain fatty acids affects disulfide bond formation in Escherichia coli and activates envelope stress response pathways as a combat strategy” in PLOS Genetics (2020) as the first author.
Author interview
How would you explain your paper’s key results to the non-scientific community?
The human body is a nutrient-rich habitat that supports various microbes, including harmful ones (pathogens). Long-chain fatty acids (LCFAs) — fats with 12 or more carbon atoms — are a rich energy source for many pathogens like Vibrio cholerae, Salmonella typhimurium, Mycobacterium tuberculosis, and Pseudomonas aeruginosa. Using E. coli, a common gut bacterium, as a model, we studied how LCFA metabolism influences bacterial functioning.
E. coli has two main cellular regions: the cytoplasm and the envelope. The envelope is the protective layer in direct contact with the environment and is crucial for many cell functions. Proteins in the envelope need disulfide bonds (links between sulfur atoms) to function properly. These bonds are formed by proteins DsbA and DsbB, which pass on electrons to ubiquinone, a component of the electron transport chain.
However, LCFA metabolism increases the flow of electrons to ubiquinone, making it less available for the DsbA-DsbB system. This impairs disulfide bond formation. Interestingly, E. coli compensates by activating a stress response pathway (called Cpx) that boosts ubiquinone levels, restoring the bond formation process.
“Our work presents the foremost instance of the integration of LCFA metabolism with cellular pathways that serve to relieve LCFA-induced problems in disulfide bond formation.”
What are the implications of your findings?
Though LCFA metabolism has long been known to boost bacterial infectivity, its interaction with other cellular processes was unclear. Our study is the first to show how LCFA metabolism interferes with disulfide bond formation and how bacteria respond to this stress. This opens avenues for future research into whether these pathways can be targeted by drugs to control bacterial infections.
What was your “Eureka!” moment?
It had been widely believed that ubiquinone is abundant and never limiting in its function. But while working on this project, I found that when E. coli is grown in LCFAs, its disulfide bond machinery becomes completely reduced, meaning it’s not working. Supplementing the cells with external ubiquinone reversed this effect. This experiment proved that ubiquinone can indeed be limiting, overturning a decades-old assumption.
What do you hope to do next?
I plan to explore two key questions:
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What molecular signal activates the Cpx pathway during LCFA metabolism?
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How exactly does the Cpx system restore disulfide bond formation?
Where do you find scientific inspiration?
I’m fascinated by how single-celled bacteria employ highly sophisticated survival strategies. Their complexity motivates me to design thoughtful experiments. My Ph.D. mentor has been a strong source of inspiration, guiding me in scientific thinking and discipline.
How do you want to contribute to Indian science?
I aim to:
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Instill scientific thinking in young minds
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Promote rational, evidence-based reasoning among the general public
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Advocate for gender equality in science
Women are underrepresented in Indian science despite earning Ph.Ds. I was fortunate to have a woman mentor, which showed me that balancing family and career is possible. I believe in creating women-support groups to help retain female talent in science and reduce the “leaky pipeline.”
Reference
Jaswal K, Shrivastava M, Roy D, Agrawal S, Chaba R (2020). Metabolism of long-chain fatty acids affects disulfide bond formation in Escherichia coli and activates envelope stress response pathways as a combat strategy. PLOS Genetics, 16(10): e1009081.
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