ATG14 and infection: In addition, mice with urothelial-cell-specific knockout of ATG16L1 (involved in phagophore elongation), ATG7 (involved in phagophore elongation), ATG14 (involved in phagophore initiation) or Epg5 (involved in autophagosome-lysosome fusion) have no effect on bacterial load in urine at an early stage (24 h post infection), while ATG16L1 and ATG7 (but not Atg14 and Epg5) deficient mice harbor fewer UPEC QIRs (quiescent intracellular reservoirs) in the bladder at 14 days post infection13.