The midblastula transition in Xenopus embryos activates multiple pathways to prevent apoptosis in response to DNA damage.

Content Provider	Semantic Scholar
Author	Finkielstein, Carla V. Lewellyn, Andrea L. Maller, James L.
Copyright Year	2001
Abstract	Apoptosis is controlled by a complex interplay between regulatory proteins. Previous work has shown that Xenopus embryos remove damaged cells by apoptosis when irradiated before, but not after, the midblastula transition (MBT). Here we demonstrate that Akt/protein kinase B is activated and mediates an antiapoptotic signal only in embryos irradiated after the MBT. In addition, an increase in xBcl-2/xBax oligomerization and a decrease in xBax homodimerization promote a protective effect against apoptosis only after the MBT. The post-MBT survival mechanism arrests cells in G(1) phase by increasing expression of the cyclin-dependent kinase inhibitor p27(Xic1). p27(Xic1) associates with cyclin D/Cdk4 and cyclin A/Cdk2 complexes to cause G(1)/S arrest, perhaps allowing more time for DNA repair. Taken together, the results define the DNA damage response as an element of the MBT and indicate that multiple mechanisms prevent apoptosis after the MBT.
Starting Page	198101
Ending Page	198101
Page Count	1
File Format	PDF HTM / HTML
Alternate Webpage(s)	http://www.pnas.org/content/98/3/1006.full.pdf
Alternate Webpage(s)	http://www.faculty.biol.vt.edu/finkielstein/docs/PNAS2001.pdf
PubMed reference number	11158585v1
Volume Number	98
Issue Number	3
Journal	Proceedings of the National Academy of Sciences of the United States of America
Language	English
Access Restriction	Open
Subject Keyword	Antiapoptotic Agent Apoptosis Cyclin A Cyclin D Cyclins DNA Damage DNA Repair Embryo Protein Kinases Proto-Oncogene Proteins c-akt negative regulation of cell cycle phase transition
Content Type	Text
Resource Type	Article