The accumulation of the compatible solute L-proline by synthesis is a cornerstone in the cell's defense against high salinity as the genetic disruption of this biosynthetic process causes osmotic sensitivity. To understand how could potentially cope with high osmolarity surroundings without the functioning of its natural osmostress adaptive L-proline biosynthetic route (ProJ-ProA-ProH), we isolated suppressor strains of mutants under high-salinity growth conditions. These osmostress-tolerant strains carried mutations affecting either the AhrC transcriptional regulator or its operator positioned in front of the L-ornithine/L-citrulline/L-arginine biosynthetic operon.
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