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Strategies for Tracking Anastasis, A Cell Survival Phenomenon that Reverses Apoptosis
12:55

Strategies for Tracking Anastasis, A Cell Survival Phenomenon that Reverses Apoptosis

Published on: February 16, 2015

Overexpression of Helicard, a CARD-containing helicase cleaved during apoptosis, accelerates DNA degradation

Magdalena Kovacsovics1, Fabio Martinon, Olivier Micheau

  • 1Institute of Biochemistry, University of Lausanne, Chemin des Boveresses 155, CH-1066, Epalinges, Switzerland.

Current Biology : CB
|May 17, 2002
PubMed

Insights

Researchers identified Helicard, a novel helicase involved in apoptosis. Upon caspase activation, Helicard translocates to the nucleus, accelerating DNA fragmentation and nuclear remodeling during programmed cell death.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Biochemistry

Background:

  • Apoptotic cell death involves nuclear changes like chromatin condensation and DNA fragmentation.
  • Caspase activation initiates these events by cleaving nuclear substrates.
  • Mitochondrial proteins AIF and endonuclease G also contribute to DNA degradation.

Purpose of the Study:

  • To identify novel proteins involved in the nuclear remodeling during apoptosis.
  • To characterize the function of a newly discovered helicase, Helicard, in the apoptotic process.

Main Methods:

  • Identification and characterization of the Helicard protein.
  • Analysis of Helicard's localization and cleavage upon apoptotic stimuli.
  • Assays to evaluate Helicard's role in DNA degradation using wild-type and mutant forms.

Main Results:

  • Helicard, a helicase with CARD domains, is widely expressed.
  • Apoptotic stimuli trigger caspase-mediated cleavage of Helicard, separating CARD and helicase domains.
  • The helicase domain translocates to the nucleus and accelerates DNA degradation.
  • Noncleavable or helicase-dead mutants impair DNA degradation, confirming Helicard's role.

Conclusions:

  • Helicard is a novel caspase-dependent nuclear helicase crucial for DNA fragmentation during apoptosis.
  • Helicard plays a significant role in nuclear remodeling associated with programmed cell death.

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