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Cheating death at the dawn of life: Developmental control of apoptotic repression in the preimplantation embryo

Journal

Publisher

ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2011.08.064

Keywords

Preimplantation embryo; Apoptosis; Cell death; DNA methylation

Funding

  1. USDA National Research Initiative [2002-35203-12664, 2007-35203-18073]
  2. BARD [US-3551-04]
  3. United States-Israel Binational Agricultural Research and Development Fund
  4. US Department of Agriculture [2004-34135-14715]

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During early development, the mammalian embryo is resistant to pro-apoptotic signals because of biochemical properties of the mitochondrion and nucleus. Mitochondria of the bovine two-cell embryo are resistant to depolarization because of low amounts of the proapoptotic protein BAX and high concentrations of the anti-apoptotic protein BCL2. As development proceeds, BAX content increases, BCL2 content declines, and mitochondria becomes capable of pore formation and depolarization in response to pro-apoptotic signals. The nucleus of the two-cell embryo is resistant to degradation by the DNase DFFB because epigenetic modifications, including DNA methylation and histone deacetylation, mask internucleosomal sites for DNA cleavage. Blastomere DNA becomes progressively less methylated during development so that DNA becomes accessible to cleavage by DFFB. (C) 2011 Elsevier Inc. All rights reserved.

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