Antitoxin component of a type V toxin-antitoxin (TA) system. Neutralizes the toxic effects of toxin GhoT by digesting ghoT transcripts in a sequence-specific manner (PubMed:22941047). In concert with GhoT is involved in reducing cell growth during antibacterial stress (PubMed:24373067). Overexpression leads to transcript level reduction of 20 other mRNAs involved in purine or pyrimidine synthesis and transport. Not seen to bind its own promoter DNA (PubMed:22941047). Monomer. Post-transcriptionally down-regulated by MqsR which acts on the ghoST transcript selectively, degrading the ghoS segment while leaving ghoT intact; conditions which induce MqsR (e.g. overexpression, nalidixic acid, azolocillin or H(2)O(2)) decrease ghoS expression and thus increase ghoT transcripts (PubMed:23289863). Unlike other TA proteinaceous antitoxins, this protein is stable with and without cellular stress; its structure has been determined in the absence of GhoT toxin. Essential; cannot be disrupted unless ghoT is also disrupted; in the double ghoS-ghoT mutant has no visible phenotype (PubMed:24373067, PubMed:22941047). Increased biofilm formation after 8 hours at 30 and 37 degrees Celsius, has risen higher by 24 hours at 37 degrees Celsius but has fallen by 24 hours at 30 degrees Celsius. Approximately 2-fold increase in swimming motility (PubMed:24373067). When single ghoT mutant is grown in the presence of antibiotics carbenicillin or cefoxitin initial metabolism is significantly increased over that of wild-type, after 14 hours wild-type is slightly less active. In a double ghoS-ghoT mutant in presence of the 2 antibiotics metabolism is significantly increased over that of wild-type, but by 9 hours wild-type has caught up and eventually has slightly greater metabolic rates (PubMed:24373067). Has a similar 3D-structure to Cas2 proteins. Can be modified to become a classic type II TA toxin (called ArT) which causes cells to become ghost-like, probably by broadening substrate RNA recognition; the toxic activity is independent of ghoT and mqsRA. Antitoxins to this evolved ArT toxin have been artificially evolved from antitoxins mqsA (a type II TA system) and toxI (a type I TA system).