Desaturase-mediated Adaptation to High Salt Concentration in Pseudomonas aeruginosa

Introduction: Bacteria have adaptation systems against environmental stresses, maintaining appropriate cell membrane fluidity for normal bacterial growth by adjusting the ratio of saturated fatty acid (SFA) and unsaturated fatty acid (UFA). One of the food spoilage bacteria, Pseudomonas aeruginosa, is usually exposed to hostile stresses such as salt in foods. In previous study, adaptability to salt in Saccharomyces cerevisiae increased by the introduction of Arabidopsis fatty acid desaturase.

Purpose: This study investigated the role of an aerobic desaturase of P. aeruginosa (DesB) on salt resistance.

Methods: Pseudomonas aeruginosa PAO1 (wild type; WT) and its derived mutants (harboring a mutation in UFA synthesis genes, such as desB, desT, desA, or fabA) were used in this study. After the bacterial cultures were exposed to osmotic stress, the growth of each mutant was compared. Transcriptional levels of WT and desB mutants through qRT-PCR analysis were compared to assess the molecular mechanism of DesB on the salt stress response. The role of DesB on salinity adaptation was phenotypically confirmed as follows: Betaine was added to medium as a complement of the osmoprotectant (NAGGN) leakage and the bacterial growth was compared.

Results: The growth of all strains was inhibited under the exposure to 0.5M or 1.0M NaCl. The desB mutant displayed more impaired growth compared to WT and other mutants, suggesting the function of DesB as a player in salt stress. Comparative transcriptional analysis showed that genes involved in the synthesis of osmoprotectants (trehalose, NAGGN, and hydrophilin) were highly expressed in WT in response to high salt, whereas rarely expressed in the desB mutant. Further, a decrease in osmoprotectant of the desB mutant was partially complemented by the addition of betaine.

Significance: The results of this study indicated that P. aeruginosa DesB played a role in adaptability to high salinity by positively regulating the synthesis of osmoprotectants.