The role of various p73 isoforms in tumorigenesis has been controversial. 
However, as we have recently shown, the generation of TAp73-deficient 
(TAp73(-/-)) mice reveals that TAp73 isoforms exert tumor-suppressive functions, 
indicating an emerging role for Trp-73 in the maintenance of genomic stability. 
Unlike mice lacking all p73 isoforms, TAp73(-/-) mice show a high incidence of 
spontaneous tumors. Moreover, TAp73(-/-) mice are infertile and produce oocytes 
exhibiting spindle abnormalities. These data suggest a link between TAp73 
activities and the common molecular machinery underlying meiosis and mitosis. 
Previous studies have indicated that the spindle assembly checkpoint (SAC) 
complex, whose activation leads to mitotic arrest, also regulates meiosis. In 
this study, we demonstrate in murine and human cells that TAp73 is able to 
interact directly with several partners of the SAC complex (Bub1, Bub3, and 
BubR1). We also show that TAp73 is involved in SAC protein localization and 
activities. Moreover, we show that decreased TAp73 expression correlates with 
increases of SAC protein expression in patients with lung cancer. Our results 
establish TAp73 as a regulator of SAC responses and indicate that TAp73 loss can 
lead to mitotic arrest defects. Our data suggest that SAC impairment in the 
absence of functional TAp73 could explain the genomic instability and increased 
aneuploidy observed in TAp73-deficient cells.