The Brn-3a/POU4F1 POU transcription factor is critical for the survival and 
differentiation of specific sensory neurons during development or upon injury; 
by regulating expression of target genes, either directly or indirectly upon 
interaction with other proteins. In this study, we demonstrated the physical 
interaction of Brn-3a with different p73 isoforms and showed co-localization in 
sensory neurons arising from the neural crest. The biological effects of p73/ 
Brn-3a interaction depend on the particular p73 isoform, because co-expression 
of Brn-3a with TAp73 enhanced cell cycle arrest, whereas Brn-3a and DeltaNp73 
cooperated to increase protection from apoptosis. Brn-3a antagonized TAp73 
transactivation of pro-apoptotic Bax, but co-operated to increase transcription 
of the cell cycle regulator p21 CIP1/Waf1. The region 425-494 amino acids within 
the TAp73 C terminus were critical for Brn-3a to repress Bax transactivation, 
but not for cooperation on the p21 CIP1/Waf1 promoter. Our results suggest that 
co-factors binding to the p73 C terminus facilitate maximal activation on the 
Bax but not p21 CIP1/Waf1 promoter and that Brn-3a modulates this interaction. 
Thus, the physical interaction of Brn-3a with specific p73 isoforms will be 
critical for determining cell fate during neuronal development or in injured 
neurons expressing both factors.