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  1. The RES domain toxins of RES-Xre toxin-antitoxin modules induce cell stasis by degrading NAD+
  2. new E. coli proteins that bind or cleave bacterial stringent response molecule (p)ppGpp
  3. Prophages and Growth Dynamics Confound Experimental Results with Antibiotic-Tolerant Persister Cells
  4. Hypothesis: type I toxin–antitoxin genes enter the persistence field—a feedback mechanism explaining membrane homoeostasis