Abstract
Apoptotic cell death has been correlated to DNA fragmentation into discrete segments corresponding to the length of nucleosomal protected fragments of 180-200 base pairs or multiples of it. This DNA degradation has been ascribed to endonuclease activity that cleaves internucleosomally, thus giving rise to a ladder distribution upon electrophoretic migration. This strict correlation was, however, shown to have notable exceptions, since in some cases only single strand cleavage in the internucleosomal DNA regions has been observed (Tomei, D. L., Shapiro, P. J., and Cope, O. F. (1993) Proc. Natl. Acad. Sci. U. S. A. 90, 853-857). In the present work we show that mouse muscle cells, able to differentiate in vitro, if subjected to apoptosis present no DNA degradation into ladder form unless differentiation is previously induced. Furthermore, C3H/10T1/2 fibroblast cells, known to undergo apoptosis without DNA ladder formation, if converted to a myogenic program by MyoD expression, display internucleosomal DNA degradation upon induction of differentiation.
Highlights
Breaks (10) or cleavage into large DNA fragments of 50 –300 kilobase pairs (11)
In the course of our studies on C2 myoblast differentiation (18) we observed that the induction of differentiation by mitogen deprivation (0.2– 0.5% fetal calf serum (FCS)) was accompanied by some cell death showing many of the characteristics of apoptosis
In this report we have described how the induction of differentiation of cultured myoblast cells alters the pattern of apoptotic DNA degradation
Summary
Breaks (10) or cleavage into large DNA fragments of 50 –300 kilobase pairs (11) (see Table 1 in Ref. 9). C3H/10T1/2 fibroblast cells, known to undergo apoptosis without DNA ladder formation, if converted to a myogenic program by MyoD expression, display internucleosomal DNA degradation upon induction of differentiation.
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
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 callDisclaimer: 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.
