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The transcription factor Zfp148 (Zbp-89, BFCOL, BERF1, htβ) interacts physically with the tumor suppressor p53 and is implicated in cell cycle control, but the physiological role of Zfp148 remains unknown. Here we show that  Zfp148  deficiency leads to respiratory distress and lethality in newborn mice.  Zfp148  deficiency prevented structural maturation of the prenatal lung without affecting type II cell differentiation or surfactant production. BrdU analyses revealed that  Zfp148  deficiency caused proliferation arrest of pulmonary cells at E18.5–19.5. Similarly,  Zfp148 -deficient fibroblasts exhibited proliferative arrest that was dependent on p53, raising the possibility that cell stress is part of the underlying mechanism. Indeed,  Zfp148  deficiency lowered the threshold for activation of p53 under oxidative conditions. Moreover, both  in vivo  and cellular phenotypes were rescued on  Trp53   +/−  or  Trp53   −/−  backgrounds and by antioxidant treatment. Thus, Zfp148 prevents respiratory distress and lethality in newborn mice by attenuating oxidative stress–dependent p53-activity during the saccular stage of lung development. Our results establish Zfp148 as a novel player in mammalian lung maturation and demonstrate that Zfp148 is critical for cell cycle progression  in vivo .

Zfp148 Deficiency Causes Lung Maturation Defects and Lethality in Newborn Mice That Are Rescued by Deletion of p53 or Antioxidant Treatment