DNA damage- and stress-induced apoptosis occurs independently of PIDD

Apoptosis. 2009 Sep;14(9):1039-49. doi: 10.1007/s10495-009-0375-1.

Abstract

The p53-induced protein with a death domain, PIDD, was identified as a p53 target gene whose main role is to execute apoptosis in a p53-dependent manner. To investigate the physiological role of PIDD in apoptosis, we generated PIDD-deficient mice. Here, we report that, although PIDD expression is inducible upon DNA damage, PIDD-deficient mice undergo apoptosis normally not only in response to DNA damage, but also in response to various p53-independent stress signals and to death receptor (DR) engagement. This indicates that PIDD is not required for DNA damage-, stress-, and DR-induced apoptosis. Also, in the absence of PIDD, both caspase-2 processing and activation occur in response to DNA damage. Our findings demonstrate that PIDD does not play an essential role for all p53-mediated or p53-independent apoptotic pathways.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis*
  • Carrier Proteins / metabolism*
  • Caspase 2 / metabolism
  • DNA Damage*
  • Death Domain Receptor Signaling Adaptor Proteins
  • Gene Targeting
  • In Situ Nick-End Labeling
  • Mice
  • Protein Processing, Post-Translational
  • Signal Transduction
  • Stress, Physiological*
  • Tumor Suppressor Protein p53 / metabolism
  • Whole-Body Irradiation

Substances

  • Carrier Proteins
  • Death Domain Receptor Signaling Adaptor Proteins
  • Pidd1 protein, mouse
  • Tumor Suppressor Protein p53
  • Caspase 2