Although the antibiotic resistance of A. baumannii has been widely studied, the transcriptional response elicited by various antibiotics in other Acinetobacter species remains poorly documented. The effects of antibiotics and the antibiotic-resistance mechanism in DR1 have been described previously, but this is first study in which the transcriptional changes induced in DR1 cells by 4 antibiotics have comparatively analyzed. Our results revealed that the MIC of Amp exhibited extremely high ranges, which could be due to high number of lactamases encoded by the DR1 genome. Amp was hydrolyzed by various b-lactamases present in the periplasm before Amp can reach its Butacaine targets. Moreover, Amp induced the genes involved in glyoxylate bypass. Glyoxylate bypass is induced in numerous bacteria when carbon and energy sources are scarce or when oxidative stress is Dimaprit dihydrochloride generated. Copper stress, which causes oxidative stress, induced glyoxylate bypass in Pseudomonas. Glyoxylate bypass was particularly induced under Amp and Nor conditions. Km strongly induced oxidative stress and caused growth defects, but could not induce glyoxylate bypass. Therefore, we speculated that there are other factors that induce glyoxylate bypass in DR1 under antibiotic conditions. In E. coli, sublethal concentrations of aminoglycosides increased the expression of several genes involved in heat-shock response, such as htpG, ibpA, groES, and asrA. Aminoglycosides also induced the Lon protease in P. aeruginosa. Our data showed that genes encoding chaperones and proteases exhibit high RPKM values under Km treatment. These results suggest that chaperones and proteases might play a key role in mistranslation under Km condition in DR1 cells. Our data showed that endonucleases did not exhibit DNA-repair capabilities in DR1 cells treated with Km and Tc. Intriguingly, only ribosome-targeting antibiotics caused a loss of DNA-repair capability; this is probably because of the long protein-maturation times required for DNA-repair enzymes. Antibiotics can interfere with the metabolic pathways of bacteria, and this can cause structural alterations in the bacterial cell wall and surface appendages including flagella, fimbriae, and pili. Bacteria employ extracellular structures such as pili and fimbriae in attachment and invasion, biofilm formation, cell motility, and transport across membranes.