In this model, the apoptosis-promoting functions
of high levels of functional p53 are balanced by the p53-mediated
transactivation of survival factors. When expression of these survival
factors is attenuated by either UV light or CHX, p53 will induce
transactivation-independent apoptosis. In addition, p53 expression
before UV irradiation increases the efficiency of survival-promoting
functions such as the recovery of mRNA synthesis. We also suggest that
previous expression of p53 protects cells against UV- or CHX-induced
apoptosis by increasing the expression of p53-regulated
survival-promoting factors before cellular stress. These protective
functions are not fully independent because stimulating the recovery of
transcription after UV irradiation will also permit the recovery of
post-UV expression of p53-regulated survival factors, thus decreasing
the induction of apoptosis. TDF, transactivation-dependent function;
TIF, transactivation-independent function; RRS, recovery of mRNA
synthesis.