Reduction of mussel metamorphosis by inactivation of the bacterial thioesterase gene via alteration of the fatty acid composition

The molecular mechanism underlying modulation of metamorphosis of the bivalve Mytilus coruscus by bacteria remains unclear. Here, the functional role of the thioesterase gene tesA of the bacterium Pseudoalteromonas marina in larval metamorphosis was examined. The aim was to determine whether inactivation of the tesA gene altered the biofilm-inducing capacity, bacterial cell motility, biopolymers, or the intracellular c-di-GMP levels. Complete inactivation of tesA increased the c-di-GMP content in P. marina, accompanied by a reduced fatty acid content, weaker motility, upregulation of bacterial aggregation, and biofilm formation. The metamorphosis rate of mussel larvae on Delta tesA biofilms was reduced by similar to 80% compared with those settling on wild-type P. marina. Exogenous addition of a mixture of extracted fatty acids from P. marina into the Delta tesA biofilms promoted the biofilm-inducing capacity. This study suggests that the bacterial thioesterase gene tesA altered the fatty acid composition of Delta tesA P. marina biofilms (BF) through regulation of its c-di-GMP, subsequently impacting mussel metamorphosis.

Automated summary

The inactivation of the tesA gene in Pseudoalteromonas marina increased the c-di-GMP content, reduced fatty acid content, weakened motility, and enhanced biofilm formation, resulting in a significant decrease in mussel larval metamorphosis rate. Addition of extracted fatty acids from P. marina to the Delta tesA biofilms promoted biofilm-inducing capacity, indicating a regulation of bacterial biofilm composition by tesA gene.