Analysis of Genes that Mediate Persistence in Halophilic Microbes Subjected to Osmotic Shock

Abstract

All organisms are subject to stress from environmental changes, and understanding the specific molecular responses to allow cells to maintain viability is a fundamental biological problem. We explore this process in the halophilic (salt‐loving) microbe Haloferax volcanii. This species was originally isolated from the Dead Sea and grows optimally at 12–14% sodium chloride. However, these organisms are regularly subjected to rapid changes in their osmotic environment during rainfall or flooding events, and we hypothesize that they have evolved so that a subset of their population consists of cells prepared to survive dramatic stress events. As a first step to examine how these ‘persisting’ cells endure, we used RNA sequencing to examine transcriptome differences in cells that survived osmotic shock compared to unstressed cells. Our data revealed that approximately half of the protein‐coding genes exhibited statistically significant differences in transcriptome abundance with a nearly equal distribution of more abundant and less abundant transcripts. There were about twice the number of transcripts exhibiting a 10‐fold or greater decrease (5.3% of protein‐coding genes) in abundance than those with the same magnitude of increased abundance (2.7% of protein‐coding genes). This result may indicate that cells primed for survival reduce production of proteins required for active metabolism. We are currently conducting experiments to determine if deletion or overexpression of some of these genes affects susceptibility of H. volcanii to osmotic shock. Our work may provide insight into why some cells in a microbial population survive stress events despite being genetically identical to cells that are killed. Similar mechanisms may also allow disease‐causing bacteria that persist even after being exposed to antibiotic agents. Potentially, the factors that carry out these responses could be targeted to enable antibiotics to effectively eliminate persister cells.Support or Funding InformationThis project was supported by an Institutional Development Award from the National Institute of General Medical Sciences (NIGMS) of the National Institutes of Health under grant P20GM103423. Additional funding was provided by the Colby College Natural Science Division.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.