Abstract
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.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callMore From: Biochemical and Biophysical Research Communications
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
