In nature, bacteria dynamically shift between a stationary (biofilm) state and a mobile (planktonic) state to maintain an ecological advantage. Within the biofilm, sedentary microorganisms are embedded in an extracellular polymeric substance (EPS), forming a protective matrix of self-produced macromolecules. These robust biofilms lead to heightened antibiotic resistance, which poses a major threat to medical and agricultural sectors. Biofilm formation and composition are heavily impacted by the nutrient sources available in the environment. We aim to understand how the transcriptome of PHL628 Escherichia coli is remodeled when exposed to L-arabinose as the sole nutrient source at 28 ºC and how that remodeling influences biofilm formation and composition. Through the examination of these modifications, affected signaling and metabolic pathways are identified that can promote or eradicate biofilms. To investigate these changes, we employ quantitative polymerase chain reactions (qPCR) to assess the expression of specific genes related to arabinose uptake and biofilm formation and transcriptome-wide analysis using RNA-seq. Notably, araE, a proton symport permease that facilitates the primary mechanism of arabinose import across the bacterial membrane, is highly upregulated in both planktonic and biofilm populations. We are also investigating the modulation of csgA and fimA, both of which encode proteins that play a role in the formation of extracellular structures that enhance bacterial adhesion to surfaces, in response to arabinose treatment. These findings characterize how L-arabinose remodels the bacterial transcriptome and provide insight into how the metabolism of this sugar intersects with the growth and composition of biofilm. We would like to acknowledge Oberlin College, The Research Corporation for Scientific Advancement, and the National Science Foundation (MCB 2226953) for supporting this research.
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Austin et al. (2024) studied this question.
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