bioRxiv Science⌕ Search

Biology subjects

Zabala-Zearreta, M.

Publications and source records attributed to Zabala-Zearreta, M..

2 recordsLinked to original sources

The cryo-EM structure of an adaptor-effector complex reveals the mechanism of a widespread pore-forming toxin family

Pseudomonas putida KT2440 is a plant-beneficial rhizobacterium that encodes multiple Type VI secretion systems (T6SS) to outcompete phytopathogens in the rhizosphere. Among its antibacterial effectors, Tke5 has been identified as a potent pore-forming toxin that disrupts ion homeostasis without causing considerable membrane damage. Tke5 belongs to the BTH_I2691 protein family and harbours an N-terminal marker for the type six secretion system effectors (MIX) motif, previously shown to be required for T6SS-dependent secretion in other systems. Many MIX-containing effectors require T6SS adaptor proteins (Tap) for secretion, but until now, the molecular mechanism for adaptor-effector binding has remained elusive. Here, we report the 2.8 [A] cryo-EM structure of the Tap3-Tke5 complex, providing structural and functional insight into how this effector is recruited by its cognate adaptor protein Tap3. Functional dissection shows that the -helical region of Tke5 is sufficient to kill intoxicated bacteria, while its {beta}-rich region likely contributes to target membrane specificity. These findings suggest a general mechanism of MIX-containing BTH_I2691 proteins for Tap recruitment and toxin activity, contributing to our fundamental understanding of a widespread yet understudied toxin family.

microbiology↗

The Pseudomonas aeruginosa Tse4 toxin assembles ion-selective and voltage-sensitive ion channels to couple membrane depolarisation with K+ efflux

Pseudomonas aeruginosa employs the Type VI secretion system (T6SS) to outcompete other bacteria in its environment. Among the effectors secreted by the T6SS of P. aeruginosa PAO1, Tse4 is known for its potent antibacterial activity. This study elucidates the molecular function of Tse4, which promotes cell depolarisation in competing bacteria. Our results show that Tse4 spontaneously incorporates into lipid monolayers and forms multiionic channels in planar bilayers, with either ohmic conduction or diode-like rectifying currents and a preference for cations over anions. These observations allow us to propose a model of action whereby Tse4 channels couple cell depolarisation with K+ efflux. These insights into Tse4s pore-forming activity enhance our understanding of bacterial competition and exemplify a finely tuned antibacterial strategy, coupling its ability to cause membrane depolarisation with potassium efflux that synergises with other T6SS effectors. These results highlight the sophistication of Pseudomonas aeruginosas competitive arsenal.

microbiology↗