Effects of temperature up-shift and UV-A radiation on fatty acids content and expression of desaturase genes in cyanobacteria Microcystis aeruginosa: stress tolerance and acclimation responses
GROWTH RATE
Fatty Acid Desaturases
Microcystis
Ultraviolet Rays
Stress, Physiological
https://purl.org/becyt/ford/1.6
Acclimatization
Fatty Acids
Temperature
M. AERUGINOSA
https://purl.org/becyt/ford/1
DESATURASES
FATTY ACIDS
DOI:
10.1007/s43630-024-00584-9
Publication Date:
2024-05-08T14:02:26Z
AUTHORS (5)
ABSTRACT
Temperature up-shift and UV-A radiation effects on growth, lipid damage, fatty acid (FA) composition and expression of desaturase genes desA and desB were investigated in the cyanobacteria Microcystis aeruginosa. Although UV-A damaging effect has been well documented, reports on the interactive effects of UV radiation exposure and warming on cyanobacteria are scarce. Temperature and UV-A doses were selected based on the physiological responses previously obtained by studies with the same M. aeruginosa strain used in this study. Cells pre-grown at 26 °C were incubated at the same temperature or 29 °C and exposed to UV-A + PAR and only PAR for 9 days. Growth rate was significantly affected by UV-A radiation independently of the temperature throughout the experiment. High temperature produced lipid damage significantly higher throughout the experiment, decreasing at day 9 as compared to 26 °C. In addition, the cells grown at 29 °C under UV-A displayed a decrease in polyunsaturated FA (PUFA) levels, with ω3 PUFA being mostly affected at the end of exposure. Previously, we reported that UV-A-induced lipid damage affects differentially ω3 and ω6 PUFAs. We report that UV-A radiation leads to an upregulation of desA, possibly due to lipid damage. In addition, the temperature up-shift upregulates desA and desB regardless of the radiation. The lack of lipid damage for UV-A on ω3 could explain the lack of transcription induction of desB. The significant ω6 decrease at 26 °C in cells exposed to UV-A could be due to the lack of upregulation of desA.
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