We thank Prof. Wood for his interest in our preprint and for noting relevant prior work. We will cite the indicated references — the 2020 amino acid resuscitation screen (iScience), the PRDP model (BBRC 2020), and the 2013 work on arrested protein synthesis and persistence (AAC)— in our revised manuscript.

We respectfully disagree, however, that our work overlaps conceptually. Using integrative metabolomics, proteomics, and genome-scale in silico flux modeling in Salmonella and other pathogens, we show that L-serine and arginine act as antagonistic signals that respectively accelerate and delay resuscitation, including within macrophages and in a murine infection model. The findings that a metabolite can actively delay awakening, and that these signals operate in pathogens during host infection, are to our knowledge new and complementary to prior nutrient-sensing work in laboratory E. coli.

We will also ensure our terminology regarding resuscitation dynamics is precise and that differing observations in the literature are appropriately discussed. We appreciate the engagement.