AS-2 specifically inhibits kinesin activity by interfering with microtubule (MT) binding, a mechanism distinct from known kinesin inhibitors. It acts as a potent toxin that can disrupt kinesin-superfamily-mediated transport when delivered intracellularly. AS-2 and its derivatives have potential applications as antimitotic or antitransport drugs for studying kinesin functions or as therapeutic agents. The existence of a kinesin atomic structure may enable the rational design of molecules based on AS-2, leading to specific inhibitors for kinesin families. AS-2 can mimic MT activity, allowing modification of surfaces or substrates to create artificial kinesin tracks. In Pseudomonas aeruginosa biofilm development, cell-to-cell signals are involved. A lasI mutant forms flat, undifferentiated biofilms that are sensitive to the biocide sodium dodecyl sulfate. These biofilms appear normal in the presence of a synthetic signal molecule. The involvement of an intercellular signal in biofilm development suggests possible targets for controlling biofilm growth in medical and industrial settings. The two signaling systems in P. aeruginosa, lasR-lasI and rhlR-rhlI, are involved in cell-to-cell communication and virulence gene expression. Quorum sensing, a form of gene regulation based on population density, is crucial for biofilm differentiation. The lasI mutant biofilm is thin and more densely packed, indicating that quorum-sensing signals are required for normal biofilm differentiation. The addition of 3OC12-HSL to the mutant biofilm rescues its structure, showing that this signal is necessary for biofilm development. The mutant biofilm is sensitive to SDS, suggesting that differentiation from planktonic cells to biofilm cells is triggered by quorum-sensing signals. The study demonstrates that cell-to-cell signals are essential for the differentiation of P. aeruginosa cells into complex structures, with implications for controlling biofilm growth in medical and industrial contexts.AS-2 specifically inhibits kinesin activity by interfering with microtubule (MT) binding, a mechanism distinct from known kinesin inhibitors. It acts as a potent toxin that can disrupt kinesin-superfamily-mediated transport when delivered intracellularly. AS-2 and its derivatives have potential applications as antimitotic or antitransport drugs for studying kinesin functions or as therapeutic agents. The existence of a kinesin atomic structure may enable the rational design of molecules based on AS-2, leading to specific inhibitors for kinesin families. AS-2 can mimic MT activity, allowing modification of surfaces or substrates to create artificial kinesin tracks. In Pseudomonas aeruginosa biofilm development, cell-to-cell signals are involved. A lasI mutant forms flat, undifferentiated biofilms that are sensitive to the biocide sodium dodecyl sulfate. These biofilms appear normal in the presence of a synthetic signal molecule. The involvement of an intercellular signal in biofilm development suggests possible targets for controlling biofilm growth in medical and industrial settings. The two signaling systems in P. aeruginosa, lasR-lasI and rhlR-rhlI, are involved in cell-to-cell communication and virulence gene expression. Quorum sensing, a form of gene regulation based on population density, is crucial for biofilm differentiation. The lasI mutant biofilm is thin and more densely packed, indicating that quorum-sensing signals are required for normal biofilm differentiation. The addition of 3OC12-HSL to the mutant biofilm rescues its structure, showing that this signal is necessary for biofilm development. The mutant biofilm is sensitive to SDS, suggesting that differentiation from planktonic cells to biofilm cells is triggered by quorum-sensing signals. The study demonstrates that cell-to-cell signals are essential for the differentiation of P. aeruginosa cells into complex structures, with implications for controlling biofilm growth in medical and industrial contexts.