p53 plays an essential pro-apoptotic role, a function thought to be shared
with its family members p73 and p63. Here, we show that p73 is primarily pr
esent in developing neurons as a truncated isoform whose levels are dramati
cally decreased when sympathetic neurons apoptose after nerve growth factor
(NGF) withdrawal. Increased expression of truncated p73 rescues these neur
ons from apoptosis induced by NCF withdrawal or p53 overexpression. In p73-
/- mice, all isoforms of p73 are deleted and the apoptosis of developing sy
mpathetic neurons is greatly enhanced. Thus, truncated p73 is an essential
anti-apoptotic protein in neurons, serving to counteract the pro-apoptotic
function of p53.