Transcriptional profiling of a Staphylococcus aureus ΔyqeK mutant under nitric oxide stress

Ap4A is produced by aminoacyl-tRNA synthetases as a byproduct of aminoacylation during stress. In other bacteria, excessive Ap4A accumulation has been linked to reduced oxidative and heat stress tolerance, increased antibiotic susceptibility, and reduced biofilm formation.

However, the role of Ap4A metabolism in S. aureus has not been characterized. Here, we show that deletion of yqeK results in Ap4A accumulation in S. aureus, which is exacerbated under stress conditions. The ΔyqeK mutant exhibits growth defects relative to wild-type during acetic acid and nitric oxide stress.