Transcriptional Response and Adaptive Evolution to Oxidative Stress in Synechococcus elongatus PCC 7942
Cyanobacteria inhabit dynamic redox environments influenced by diurnal cycles, environmental fluctuations, and nutrient availability, necessitating tight redox regulation. This RNA-seq study examines transcriptional regulation of redox control in the model cyanobacterium Synechococcus elongatus PCC 7942 under controlled turbidostatic conditions. We manipulated oxygen concentrations to generate oxidative stress across distinct phases, measuring impacts on growth, physiology, and genome-wide gene expression. Transcriptional profiling reveals independently regulated gene modules that define graded transcriptional responses aligned with redox-regulated patterns activated under fluctuating light conditions. Our findings demonstrate a coordinated, multi-phase response involving ROS formation, detoxification, and damage repair. Oxidative stress induces transcriptional repression of essential cellular processes. This dataset includes wild-type strains under acute oxidative stress and experimentally evolved populations that underwent multiple rounds of elevated oxygen exposure. The evolved strains demonstrated improved tolerance to elevated oxygen levels, enhanced sucrose productivity under high-stress conditions, and accumulated DNA mutations in genes related to molybdopterin biosynthesis and glycogen metabolism. Overall design: Time-series transcriptional analysis of S. elongatus PCC 7942 CscB/SPS strain examining both acute oxidative stress response and adaptive evolution under controlled turbidostatic conditions. Oxygen concentrations were systematically manipulated to increase oxidative stress and define distinct phases of inhibition impacting growth, physiology, and gene expression. The starting wild-type (WT) population was grown between 0-78.4% oxygen before being transferred to 0% oxygen, establishing baseline stress response patterns. This oxygen stress cycle was repeated in adapted population one (0-93% oxygen cycling to 0%) and adapted population two (0-99.8% oxygen cycling to 0%). A final sample was collected at 0% oxygen for adapted population 3. Each adapted population was derived from the previous population, representing progressive adaptation to increasingly severe oxidative stress. Through transcriptional analysis at multiple time points across these populations, we identified independently regulated gene set modules revealing coordinated multi-phase responses to ROS formation, detoxifying ROS, and repairing damage. Multiple rounds of induced oxidative stress resulted in adaptive mutations and evolved phenotypes. Two technical replicates were analyzed for each condition sample.