Survivin is a member of the inhibitor apoptosis family that is overexpressed in 
many malignancies. It has five known alternative splice forms, some of which 
differ in their antiapoptotic properties and expression levels in human cancers. 
Here we describe a novel donor splice site (DSS), 2B+32 DSS, which is used in 
conjunction with survivin alternative exon 2B, resulting in the inclusion of 32 
additional nucleotides from intron 2 at the 3' end of this exon. Sequence 
analysis showed that both the classical exon 2B DSS and 2B+32 are provided by an 
Alu sequence, which is inserted in intron 2 downstream of a functional acceptor 
splice site, leading to the exonization of part of the repetitive element. Minor 
transcripts including the 2B+32 alternative exon, or retaining the whole 
intronic region comprised between exons 2B and 3, were detected in several human 
cell lines and in some human tissues. Survivin 2B+32 containing variants acquire 
a premature stop codon (PTC) and may therefore be degraded by the nonsense 
mediated decay pathway. The implication of these novel isoforms, as well as 
other PTC+ survivin variants, in the overall regulation of survivin expression 
is discussed. Sequence analysis of intron 2 which contains the Alu Y element was 
performed on different primate species in order to trace its insertion and 
exonization during primate evolution.