Key result
Avian leukosis virus proviruses with an inactivating mutation in the poly(A) addition signal utilized functional polyadenylation sites within flanking cell DNA and cryptic sites within viral sequences.
The study demonstrates that readthrough transcripts are a general property of retroviral integration and that mutations in the poly(A) signal lead to the use of alternative polyadenylation sites in flanking cell DNA and cryptic viral sites.
May affect retroviral transcript processing in models; leaves open extension to human gene therapy or cardiovascular applications.
Readthrough transcripts are formed during retrovirus infection by polyadenylation of viral RNA in cellular sequences adjacent to the provirus. We have studied such transcripts in avian leukosis virus-infected cell clones containing a single provirus, either the wild type or one with an inactivating mutation in the poly(A) addition signal. All individual wild-type proviruses produced readthrough transcripts, implying that this property is not restricted to a few integration sites. The range of sizes of viral RNA in the mutant lacking a correct signal for poly(A) addition reflected both the occurrence of functional polyadenylation sites within flanking cell DNA and increased usage of cryptic sites within viral sequences.
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Swain et al. (1993) studied Avian leukosis virus infection. Inactivating mutation in the poly(A) addition signal vs. Wild type provirus was evaluated on Readthrough transcripts and polyadenylation site usage. Avian leukosis virus proviruses with an inactivating mutation in the poly(A) addition signal utilized functional polyadenylation sites within flanking cell DNA and cryptic sites within viral sequences.
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