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Biofilm formation genes comprise a diverse functional group of bacterial and fungal genes that regulate the transition from a motile planktonic state to a sessile, multicellular community. These genes are responsible for the various stages of biofilm development, including initial surface attachment (e.g., adhesins like fnbA), the production of the extracellular polymeric substance (EPS) matrix (e.g., the icaADBC operon in Staphylococcus or alg/psl/pel genes in Pseudomonas), and the regulation of community behavior through quorum sensing systems like luxS or lasR (Hall & Mah, 2017; Roy et al., 2018). Biofilms serve as a protective niche that shields pathogens from the host immune system and increases antibiotic tolerance by up to 1000-fold compared to planktonic cells (Jamal et al., 2018). In clinical settings, biofilm formation genes are critical drivers of chronic and recalcitrant infections, particularly those associated with medical implants, cystic fibrosis, and chronic wounds. Therapeutic strategies targeting these genes aim to inhibit the signaling pathways (quorum sensing inhibitors), degrade the physical matrix (enzymes like DNase I or Dispersin B), or prevent initial colonization. Because these genes represent a broad class of diverse molecular entities across different species rather than a single distinct receptor, they are often addressed as a metabolic pathway or a collective virulence factor in drug development (Roy et al., 2018; Jamal et al., 2018).
Inhibition of quorum sensing (QS) signaling, degradation of extracellular polymeric substances (EPS) such as eDNA or polysaccharides, inhibition of initial bacterial adhesion to surfaces, and interference with secondary messengers like cyclic-di-GMP.
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