Yamauchi Y, Tanaka A, Hanaoka F, Okumura K
Cellular Physiology Laboratory, Institute of Physical and Chemical Research (RIKEN), Saitama, Japan.
Biochem Biophys Res Commun. 1998 Feb 13;243(2):550-4. doi: 10.1006/bbrc.1998.8121.
A mutant strain of mouse FM3A cells was defective in apoptotic DNA fragmentation. Upon DNA damage by UV-radiation, the strain did not form DNA fragments, though it accumulated a large amount of p53 protein as did wild-type cells. No DNA fragmentation was observed when the strain was subjected to other kinds of DNA damaging agents such as X ray-radiation, or addition of etoposide to the culture medium. Other well-known biological stimulations inducing apoptosis, serum depletion or addition of TNF-alpha to the culture medium, also failed to cause DNA fragmentation in the cells. Using this apoptosis-deficient strain, we characterized another apoptotic reaction, export of phosphatidylserine to the cell surface. This molecule was exported onto the surface in both wild-type and the mutant cells when cells were treated with TNF-alpha and cycloheximide. Thus, the export of phosphatidylserine is suggested to be independent of the pathway for apoptotic DNA fragmentation.
