Promotes alternative splicing of late transcripts by promoting splicing at weak 3' splice sites. Required for the temporal activation of major late pre-mRNA splicing at late times of infection. Induces the splicing and expression of the late capsid vertex protein (By similarity). Probably functions as the small terminase that is part of the molecular motor that translocates genomic DNA in empty capsid during DNA packaging. This motor is located at a unique vertex and comprises at least the IVa2 ATPase, the small terminase 33K and probably a portal. Forms a ring-like structure of about 17 nm in which genomic DNA is translocated into the capsid. Stimulates IVa2 ATPase activity in the presence of the viral genome. Once the DNA is packaged, the terminase detaches: the 33K protein is present in the empty particles, but not in the mature virions. Also involved in virion assembly. Homooligomer. Interacts with DBP; this interaction occurs at a unique vertex during genome packaging. Interacts with IVa2; this interaction occurs at a unique vertex during genome packaging and seems to potentiate IVa2 and 33K oligomerization. At late time of infection, reorganized from the nuclear margin to ring-like structures at viral replication centers. Expressed in the late phase of the viral replicative cycle. The tiny Arg-Ser repeat region (RS repeat) is necessary for the splicing enhancer function. Phosphorylated in vitro by human PKA and PRKDC. PRKDC inhibits, whereas PKA activates the splicing factor (By similarity). All late proteins expressed from the major late promoter are produced by alternative splicing and alternative polyadenylation of the same gene giving rise to non-overlapping ORFs. Expression of packaging protein 2 and splicing factor is controlled by a L4 promoter distinct from the major late promoter (By similarity). Spliced isoform. Unspliced isoform. Belongs to the adenoviridae splicing factor family.