Abstract
A mutation of the Drosophila melanogaster vermilion (v) gene known as v(1) is caused by the insertion of a 412 retrotransposon into the 5' untranslated region of the first exon. Mutants carrying this insertion accumulate a low level of mRNA from which most of the transposon sequences have been eliminated by splicing at cryptic sites within transposon sequences. Here, we demonstrate that a revertant of the v(1) allele called v(+37) is caused by the insertion of a second retrotransposon, the B104/roo element, into a site near one end of the 412 element. The revertant strain accumulates a higher level of mRNA from which most of both transposons have been removed by splicing at new donor sites introduced by the B104/roo insertion and the same acceptor site within 412. Mutations at suppressor of sable [su(s)], which increase the accumulation of v(1) transcripts, slightly elevate the level of v(+37) RNA. In addition, we show that the first v intron downstream of the 412 insertion is not efficiently removed in the v(1) mutant, and suppressor and reversion mutations increase the proportion of transcripts that are properly spliced at that downstream intron. Thus, it appears that both the suppressor and reversion mutations exert an effect at the level of pre-mRNA splicing.
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Selected References
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